ABSTRACT
Antecedentes y objetivo: La gravedad e inestabilidad de los pacientes, junto con el alto grado de complejidad de la medicación, hacen de las unidades de cuidados intensivos (UCI) un área crítica de problemas relacionados con la medicación. El objetivo de nuestro estudio fue analizar y evaluar la actividad clínica realizada por el farmacéutico clínico integrado en una UCI y conocer la opinión del personal. Material y método: Estudio descriptivo, prospectivo, de 42 meses de duración. El farmacéutico se integró en la actividad diaria del equipo multidisciplinar de una UCI de 12 camas perteneciente al Servicio de Anestesiología y Reanimación. Se registraron todas las intervenciones farmacoterapéuticas (IF) realizadas, el grado de aceptación, el método de comunicación y destinatario de la intervención, así como la evaluación clínica de las intervenciones aceptadas. Posteriormente, se realizó una encuesta al personal de la unidad sobre la seguridad del paciente y la influencia de la integración del farmacéutico en la unidad. Resultados: Se realizaron un total de 2399 IF con un 97,0% de aceptación. De estas, las mayoritarias fueron las relacionadas con la posología (37,8%) y las consultas al farmacéutico (25,7%). De las IF aceptadas, el 53,7% influyeron sobre la eficacia del tratamiento farmacológico y el 35,1% sobre la tolerancia. En la encuesta realizada al personal de la unidad para valorar la percepción de la integración del farmacéutico se obtuvo una valoración global de de 8,58 ± 1,40 sobre 10. Conclusiones: El farmacéutico hospitalario integrado en el equipo multidisciplinar de UCI puede aportar un valor añadido al proceso farmacoterapéutico del paciente crítico
Background and objective: The severity and instability of the patients, together with the high degree of complexity of the medication, make the intensive care units (ICU) a critical area of problems related to medication. The aim of our study was to analyze and assess the activity performed by the clinical pharmacist integrated in an ICU and to know the opinion of the staff about it. Material and method: A 42 month descriptive and prospective study was conducted. The pharmacist was integrated into the daily activity of the multidisciplinary team of a 12-bed ICU belonging to the Anaesthesiology and Resuscitation Department. Every pharmacotherapeutic intervention (PI) carried out, the degree of acceptance, the method of communication and the receiver of the intervention, as well as the clinical evaluation of the accepted interventions were recorded. Subsequently, a survey was carried out to the staff of the unit on the patient's safety and the influence of the integration of the pharmacist in the unit. Results: A total of 2399 PIs were carried out with a 97.0% of acceptance. Of these, most were those related to posology (37.8%) and consultations with the pharmacist (25.7%). Among the accepted PIs, 53.7% had an influence on the efficacy of drug therapy, and 35.1% on treatment tolerance. In the survey to the unit's staff in order to assess the perception of the pharmacist's integration, an overall assessment of 8.58 ± 1.40 out of 10 was obtained. Conclusions: The hospital pharmacist integrated in the ICU multidisciplinary team can add value to the pharmacotherapeutic process of the critical patient
Subject(s)
Humans , Patient Care , Critical Illness , Pharmaceutical Services/methods , Critical Care , Pharmacy/trends , Pharmaceutical Services , Prospective Studies , Patient Safety , Intensive Care UnitsABSTRACT
We describe a recent case of Stevens-Johnson Syndrome. A 49-year-old man was admitted to the Intensive Care Unit of an Anaesthesia and Resuscitation Department because of a Fournier gangrene that derived in a sepsis, ventilator-associated pneumonia, and renal failure. He was under treatment with cefepime and suffered a generalized status epilepticus, so started treatment with phenytoin. The next day he developed a "maculous cutaneous eruption in trunk and lower limbs" compatible with a Stevens-Johnson Syndrome. Stevens-Johnson Syndrome is a very severe and potentially fatal multiorganic disease, especially when present in critically ill patients, with a strong drug-related etiology, especially with antiepileptic drugs.
Subject(s)
Anti-Bacterial Agents/adverse effects , Anticonvulsants/adverse effects , Cephalosporins/adverse effects , Phenytoin/adverse effects , Stevens-Johnson Syndrome/therapy , Anticonvulsants/therapeutic use , Cefepime , Critical Illness , Fournier Gangrene/complications , Fournier Gangrene/drug therapy , Humans , Kidney Failure, Chronic/complications , Male , Middle Aged , Phenytoin/therapeutic use , Pneumonia, Ventilator-Associated/complications , Pneumonia, Ventilator-Associated/drug therapy , Sepsis/complications , Sepsis/drug therapy , Status Epilepticus/chemically induced , Status Epilepticus/drug therapy , Stevens-Johnson Syndrome/etiologyABSTRACT
Minocycline, an antibiotic of the tetracycline family, has attracted considerable interest for its theoretical therapeutic applications in neurodegenerative diseases. However, the mechanism of action underlying its effect remains elusive. Here we have studied the effect of minocycline under excitotoxic conditions. Fluorescence and bioluminescence imaging studies in rat cerebellar granular neuron cultures using fura2/AM and mitochondria-targeted aequorin revealed that minocycline, at concentrations higher than those shown to block inflammation and inflammation-induced neuronal death, inhibited NMDA-induced cytosolic and mitochondrial rises in Ca(2+) concentrations in a reversible manner. Moreover, minocycline added in the course of NMDA stimulation decreased Ca(2+) intracellular levels, but not when induced by depolarization with a high K(+) medium. We also found that minocycline, at the same concentrations, partially depolarized mitochondria by about 5-30 mV, prevented mitochondrial Ca(2+) uptake under conditions of environmental stress, and abrogated NMDA-induced reactive oxygen species (ROS) formation. Consistently, minocycline also abrogates the rise in ROS induced by 75 microM Ca(2+) in isolated brain mitochondria. In search for the mechanism of mitochondrial depolarization, we found that minocycline markedly inhibited state 3 respiration of rat brain mitochondria, although distinctly increased oxygen uptake in state 4. Minocycline inhibited NADH-cytochrome c reductase and cytochrome c oxidase activities, whereas the activity of succinate-cytochrome c reductase was not modified, suggesting selective inhibition of complexes I and IV. Finally, minocycline affected activity of voltage-dependent anion channel (VDAC) as determined in the reconstituted system. Taken together, our results indicate that mitochondria are a critical factor in minocycline-mediated neuroprotection.
