ABSTRACT
Acute kidney injury (AKI) is a growing concern in Intensive Care Units. The advanced age of our patients, with the increase in associated morbidity and the complexity of the treatments provided favor the development of AKI. Since no effective treatment for AKI is available, all efforts are aimed at prevention and early detection of the disorder in order to establish secondary preventive measures to impede AKI progression. In critical patients, the most frequent causes are sepsis and situations that result in renal hypoperfusion; preventive measures are therefore directed at securing hydration and correct hemodynamics through fluid perfusion and the use of inotropic or vasoactive drugs, according to the underlying disease condition. Apart from these circumstances, a number of situations could lead to AKI, related to the administration of nephrotoxic drugs, intra-tubular deposits, the administration of iodinated contrast media, liver failure and major surgery (mainly heart surgery). In these cases, in addition to hydration, there are other specific preventive measures adapted to each condition
La lesión renal aguda (LRA) constituye un problema de importancia creciente en las unidades de cuidados intensivos. La mayor edad de nuestros pacientes, con el aumento de la morbilidad asociada, y la complejidad de los tratamientos realizados favorecen su desarrollo. Puesto que la LRA carece de tratamiento eficaz, todos los esfuerzos se dirigen a la prevención y a su detección precoz con el fin de establecer medidas de prevención secundaria que impidan su progresión. En el paciente crítico, las causas más frecuentemente implicadas son la sepsis y las situaciones que provocan hipoperfusión renal, por lo que las medidas preventivas irán encaminadas a mantener un estado de hidratación y hemodinámico correcto mediante perfusión de fluidos y el uso de fármacos inotrópicos o vasoactivos en función de la enfermedad subyacente. Además de estas circunstancias, existen distintas situaciones que pueden favorecer la LRA, relacionadas con la administración de fármacos nefrotóxicos, los depósitos intratubulares, la administración de contrastes iodados, el fallo hepático y la cirugía mayor, fundamentalmente cirugía cardiaca. En estos casos, además de la hidratación, se dispone de otros aspectos preventivos específicos de cada entidad
Subject(s)
Humans , Acute Kidney Injury/prevention & control , Sepsis/prevention & control , Water-Electrolyte Imbalance/prevention & control , Critical Care/methods , Secondary Prevention/methods , Fluid TherapyABSTRACT
Acute kidney injury (AKI) is a growing concern in Intensive Care Units. The advanced age of our patients, with the increase in associated morbidity and the complexity of the treatments provided favor the development of AKI. Since no effective treatment for AKI is available, all efforts are aimed at prevention and early detection of the disorder in order to establish secondary preventive measures to impede AKI progression. In critical patients, the most frequent causes are sepsis and situations that result in renal hypoperfusion; preventive measures are therefore directed at securing hydration and correct hemodynamics through fluid perfusion and the use of inotropic or vasoactive drugs, according to the underlying disease condition. Apart from these circumstances, a number of situations could lead to AKI, related to the administration of nephrotoxic drugs, intra-tubular deposits, the administration of iodinated contrast media, liver failure and major surgery (mainly heart surgery). In these cases, in addition to hydration, there are other specific preventive measures adapted to each condition.
Subject(s)
Acute Kidney Injury/prevention & control , Critical Care/methods , Intensive Care Units , Acute Kidney Injury/etiology , Acute Kidney Injury/physiopathology , Acute Kidney Injury/therapy , Contrast Media/adverse effects , Diuretics/therapeutic use , Fenoldopam/therapeutic use , Fluid Therapy , Hemodynamics , Humans , Liver Failure/complications , Liver Failure/therapy , Postoperative Complications/prevention & control , Renal Circulation/drug effects , Rhabdomyolysis/complications , Rhabdomyolysis/therapy , Risk Factors , Secondary Prevention , Sepsis/complications , Sepsis/therapy , Vasoconstrictor Agents/adverse effectsABSTRACT
A procedure for calibrating a Clark-type oxygen electrode is described. This method is based on the oxidation of 4-tert-butylcatechol (TBC) by O2 catalyzed by tyrosinase, to yield 4-tert-butyl-o-benzoquinone (TBCQ). This reaction consumes known amounts of oxygen in accordance with the stoichiometry: 2TBC + O2----2TBCQ + 2H2O and can be used to determine the relation between the oxygen concentration and the oxygen electrode response. TBCQ is very stable in the reaction medium for more than 30 min and shows no significant breakdown, which makes the calibration possible. A kinetic study of the oxidation of 3,4-dihydroxyphenylalanine by tyrosinase using the oxygen electrode is shown to confirm the validity of the calibration method.
