ABSTRACT
Los pacientes quemados pueden necesitar ingresos prolongados en el Servicio de Medicina Intensiva, tanto para la atención inicial como para el tratamiento pre y postoperatorio de las múltiples cirugías que precisan. La reanimación inicial del paciente quemado crítico requiere una adecuada monitorización para calcular la fluidoterapia necesaria para reponer las pérdidas y asegurar la perfusión tisular, pero sin excesos que aumenten el edema intersticial. Además, la monitorización puede evaluar la respuesta inflamatoria sistémica, que puede llevar a shock y a disfunciones orgánicas. Tras esta fase inicial nos encontraremos con un paciente crítico que requiere múltiples reintervenciones en situaciones no óptimas, por lo que necesitará cuidados especiales durante un largo periodo. Además, el Servicio de Medicina Intensiva ofrece la atención postoperatoria específica para la cirugía reconstructiva y el trasplante de tejidos compuestos (miembro superior y cara), en los que el éxito depende de un riguroso control mediante la monitorización y el tratamiento adecuados
Burned patients may need prolonged admissions in the Intensive Care Service, both for initial care and for the pre and postoperative treatment of the multiple surgeries they require. The initial resuscitation of critically burned patients requires adequate monitoring to calculate the fluid therapy necessary to replenish the losses and ensure tissue perfusion, but without excesses that increase interstitial edema. In addition, monitoring can evaluate the systemic inflammatory response that can lead to shock and organic dysfunctions. After this initial phase we will find a critical patient who requires multiple reinterventions in non-optimal situations, so he will need special care over a long period of time. In addition, the Intensive Care Service offers specific postoperative care for reconstructive surgery and the transplantation of composite tissues (upper limb and face) in which its success depends on a rigorous control through adequate monitoring and treatment
Subject(s)
Humans , Burns, Electric/surgery , Perioperative Period/methods , Plastic Surgery Procedures/methods , Intensive Care Units , Critical Care/methods , Fluid Therapy , Postoperative Care , Surgical Flaps , Thermodilution/methods , Pain Management , Ascorbic Acid/administration & dosage , Preoperative PeriodABSTRACT
Burned patients may need prolonged admissions in the Intensive Care Service, both for initial care and for the pre and postoperative treatment of the multiple surgeries they require. The initial resuscitation of critically burned patients requires adequate monitoring to calculate the fluid therapy necessary to replenish the losses and ensure tissue perfusion, but without excesses that increase interstitial edema. In addition, monitoring can evaluate the systemic inflammatory response that can lead to shock and organic dysfunctions. After this initial phase we will find a critical patient who requires multiple reinterventions in non-optimal situations, so he will need special care over a long period of time. In addition, the Intensive Care Service offers specific postoperative care for reconstructive surgery and the transplantation of composite tissues (upper limb and face) in which its success depends on a rigorous control through adequate monitoring and treatment.
Subject(s)
Burns/therapy , Critical Care , Perioperative Period , Burns/complications , Cardiac Output/physiology , Fluid Therapy/methods , Humans , Monitoring, Physiologic/methods , Postoperative Care/methods , Plastic Surgery Procedures/adverse effects , Plastic Surgery Procedures/methods , Replantation/methods , Sepsis/complications , Smoke Inhalation Injury/complicationsSubject(s)
Anesthetics, Combined , Anesthetics, Intravenous , Ophthalmoplegia, Chronic Progressive External/chemically induced , Piperidines , Propofol , Ambulatory Surgical Procedures , Female , Humans , Malignant Hyperthermia/prevention & control , Middle Aged , Mitochondrial Myopathies , RemifentanilABSTRACT
Results of many clinical and experimental studies indicate an inverse relationship between dietary calcium and the prevalence of hypertension. Our study was designed to evaluate the alterations in arterial blood pressure and the changes in alpha-adrenoceptor-mediated vascular reactivity in normotensive Sprague-Dawley and spontaneously hypertensive rats (SHR) fed from weaning (3 weeks of life) three diets: normal calcium (Ca 1%), low calcium (Ca 0.1%), and high calcium (Ca 2.5%). The systolic and the diastolic arterial blood pressures were measured weekly by the tail cuff method. The plasma calcium levels in the animals were also measured regularly by colourimetric methods, and the alpha-adrenoceptor-mediated vascular reactivity was evaluated by measuring the pressor responses to alpha-adrenoceptor agonists in pithed rats. These determinations were carried out at the end of the feeding periods (9 weeks of life in Sprague-Dawley rats and 20 weeks of life in SHR) and also at the moments when maximal differences in arterial blood pressure were observed between the conscious animals fed the normal calcium diet and those fed the other two diets. Dietary calcium deficiency increased arterial blood pressure in both strains but calcium supplements were effective to lower this only in hypertensive animals. The plasma calcium levels were altered in both strains when calcium administration was not normal. The low-calcium diet did not modify the pressor responses to either the alpha(1)-adrenoceptor agonist, methoxamine, or the alpha(2)-adrenoceptor agonist, B-HT 920 (5-allyl-2-amino-5,6,7, 8-tetrahydro-4H-thiazolo-(4,5-D)-acepin-dihydrochloride, talixepole), in the normotensive and the hypertensive rats. On the contrary, the high-calcium diet caused a definite decrease in alpha(1)- and alpha(2)-adrenoceptor-mediated vascular reactivity in both strains. The changes in the alpha-adrenoceptor-mediated vasoconstrictor responses were observed in pithed 9-week old Sprague-Dawley rats and in pithed 20-week old SHR, but none were observed in pithed 15-week old SHR, although at this age maximal differences in arterial blood pressure between the animals fed the high- and the normal calcium diet were observed. The results of this study suggest that the mechanisms implicated in the effects of dietary calcium supplements on arterial blood pressure are clearly different from the mechanisms, which bring about changes in arterial blood pressure when the diet is deficient in calcium. The results of this study also show that calcium administration causes variations in alpha-adrenoceptor-mediated vascular reactivity, but this is probably not the only mechanism implicated in the calcium effect on arterial blood pressure.
Subject(s)
Blood Pressure/drug effects , Calcium, Dietary/administration & dosage , Receptors, Adrenergic, alpha/physiology , Adrenergic alpha-Agonists/pharmacology , Animals , Azepines/pharmacology , Calcium/blood , Decerebrate State , Diastole , Diet , Dose-Response Relationship, Drug , Male , Methoxamine/pharmacology , Rats , Rats, Inbred SHR , Rats, Sprague-Dawley , Receptors, Adrenergic, alpha/drug effects , SystoleABSTRACT
Hypertension caused by calcium deficiency in the diet has been linked with an increase in parathyroid hormone (PTH) and calcitriol levels. We evaluated arterial blood pressure (ABP), PTH, and calcitriol in normotensive Sprague-Dawley rats (SDR) and in spontaneously hypertensive rats (SHR) fed from weaning on a control diet with a normal calcium content (1%) or a low-calcium diet (0.1%). The calcemia was also measured in the rats by colorimetric methods. The low-calcium diet decreased the calcemia in both strains and brought about an increase in the ABP which was significant in adult SDR and particularly noticeable during the early hypertensive phase in SHR. The rats fed on this diet had higher hormonal plasma levels when compared with the corresponding values in rats fed on the control diet. In particular, the SDR fed on the low-calcium diet showed much higher PTH (122.6 +/- 31.0 pg/ml, p = 0.05) and calcitriol (458.0 +/- 13.1 pg/ml, p = 0.01) values than the SDR fed on the control diet (PTH 31.7 +/- 2.80 pg/ml; calcitriol 292.1 +/- 17.5 pg/ml). These endocrine alterations could justify the increase in ABP caused by dietary calcium deficiency in normotensive rats. Nevertheless, the results of this study indicate that the modifications of the ABP caused by the low-calcium diet in SHR could not be correlated with significant increases in these hormones.