Distrofia simpático refleja o síndrome de dolor regional complejo tipo I / Reflex sympathetic dystrophy or complex regional pain syndrome type I

La distrofia simpático refleja es una entidad que engloba diferentes situaciones patológicas caracterizada por dolor, alteraciones vaso, sudomotoras y cambios tróficos. La etiología es variopinta, destacando la cirugía, lesión por aplastamiento, fracturas y esguinces como causas más frecuentes, localizándose sobre todo en la parte distal de ambas extremidades. Fisiopatológicamente se cree que cambios estructurales a nivel nervioso periférico, en los ganglios y en el asta dorsal de la médula, junto con una actividad simpática exagerada, condicionan que las fibras nociceptivas se activen de forma anómala espontánea y repetitivamente. Los pacientes refieren dolor, alodinia, hiperestesia, cambios de coloración y temperatura de la extremidad; hiperhidrosis y cambios tróficos en los anejos de la piel. Clásicamente se describen tres fases: aguda o caliente, fría o distrófica y atrófica. El diagnóstico se basa fundamentalmente en la clínica y la exploración física. Ninguna prueba diagnóstica resulta concluyente excepto la desaparición del dolor tras el bloqueo simpático.La terapia farmacológica consiste en la utilización de antidepresivos, anestésicos locales, vasodilatadores, betabloqueantes, bloqueantes del calcio y sobre todo, los nuevos anticomiciales (gabapentina y topiramato).Ante el fracaso de ésta se puede recurrir a los bloqueos simpáticos (ganglio estrellado, regional intravenosos, epidurales). Otras técnicas consisten en la realización de simpatectomías quirúrgicas, bloqueos neurolíticos, estimulación de cordones posteriores o lesiones neuroquirúrgicas en los casos refractarios a otros tratamientos (AU)

Complicaciones en cirugía oftalmológica secundarias a cambio de aguja retrobulbar / Complications of eye surgery with use of a retrobulbar needle

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Transabdominal surgical approach in the management of renal tumors involving the retrohepatic inferior vena cava.

Multiple reports over the last decade have documented the clear superiority of surgery over other alternative treatments in the management of renal cell carcinoma with extension into the inferior vena cava (IVC). Controversy persists, however, regarding the management of tumor thrombus that extends retrohepatically, but not entering the right atrium. In this report, we retrospectively review our experience with the use of a feasible transabdominal technique without any form of bypass or anticoagulation for safe removal of renal tumor involving the retrohepatic IVC. From 1988 to 1998, 132 patients with renal cell carcinoma underwent radical nephrectomies at the urology service of our hospital. Five patients (3.8%) had retrohepatic venous extension through the renal vein into the IVC. Our transabdominal approach was accomplished by complete mobilization of the liver, control of the hepatocaval connection, total vascular exclusion of the IVC without heparin administration, removal of the tumor thrombus, and primary closure of the longitudinal vena cavotomy. From our results, we found the transabdominal approach with total vascular exclusion of the IVC to be satisfactory, with no early deaths, acceptable morbidity, and a remarkable limitation of blood loss and transfusion requirements.

[Subtypes of muscarinic acetylcholine receptor following the experimental denervation of the cholinergic pathway ascending to the neocortex]. / Subtipos del receptor muscarínico de acetilcolina tras la denervación experimental de la vía colinérgica ascendente al neocórtex.

BACKGROUND: Use of an experimentally induced neurotoxic lesion of the ascending cholinergic pathway to the neocortex, in rat brain, to study the postulated selective loss of muscarinic receptor subtypes (mAChR) presynaptically located (autoreceptors). METHODS: Stereotaxic lesion of n. basalis magnocellularis was induced by 25 nmol Ibotenic acid injection in the right brain hemisphere of adult, male, Wistar rats. The contralateral hemisphere served as control. Antagonist (quinuclidinyl-benzilate) and agonist (carbachol) specific binding to mAChR receptors at equilibrium was studied 7 days post-lesion on a P2 fraction of brain cortex homogenate. Displacement of antagonist binding by carbachol was analyzed by "one-point" and "two-point" model fits. RESULTS: Muscarinic receptors on the control hemisphere show no sign of lesion related changes as compared to data for intact rat brain: Bmax = 0.896 pmol/mg protein and Kd = 0.25 nM. In the lesioned hemisphere a -10.3% loss of antagonist binding (not statistically significant) was observed, with an increase in receptor affinity. Heterogeneity of agonist binding was found; receptor subtype analysis showed that the proportion M2/M1 was unchanged but an increase in carbachol (M2 selective affinity) did appeared. CONCLUSIONS: We found no evidence of a selective presynaptic localization of muscarinic receptor sub-types on terminals of the cholinergic ascending pathway to the neocortex. A receptor loss related to the intensity of the neurotoxic lesion is suggested as well as the presence of regulative mechanisms (hypersensitivity) for receptors.