Concordancia entre las ecuaciones de estimación del filtrado glomerular y el aclaramiento de creatinina en orina de 4horas en pacientes críticos con trauma grave / Concordance between glomerular filtration rate estimation equations and 4-hour urinary creatinine clearance in critically ill patients with severe trauma

Antecedentes y objetivo: Cada vez hay más estudios que evidencian que las ecuaciones utilizadas para conocer la tasa de filtrado glomerular estimada (TFGe) no son adecuadas para los pacientes críticos en los que se producen continuas variaciones del filtrado glomerular (FG). El método más práctico para aproximarse al estudio del FG es el cálculo del aclaramiento de creatinina (ClCr) en periodos de recogida de orina variables. El objetivo del estudio fue observar el comportamiento de las ecuaciones empleadas para estimar el filtrado glomerular cuando se aplican a la subpoblación de pacientes críticos ingresados por trauma grave y comparar el ClCr en orina recogida en un periodo de 4horas (ClCr-4h). Material y métodos: Estudio observacional que incluye pacientes ingresados por trauma grave. Se calculó el ClCr-4h y se determinó la TFGe mediante las ecuaciones de Cockcroft-Gault, Jelliffe modificada, MDRD, t-MDRD y CKD-EPI. Los resultados se expresan referidos a superficie corporal (ml/min/1,73m2). Los análisis se realizaron con el software estadístico R versión 4.0.4. Resultados: Se incluyeron 85 pacientes. La edad mediana de los pacientes fue de 51años; 68 pacientes fueron varones (78,82%). El ClCr-4h ajustado a superficie corporal (ClCr-4h ml/min/1,73m2) medio fue de 84,5ml/min/1,73m2. Hallamos correlación estadísticamente significativa de ClCr-4h/1,73m2 con la TFGe por t-MDRD. Para ClCr-4h/1,73m2 mayores de 130ml/min/m2 la ecuación de Cockcroft-Gault identifica a los pacientes correctamente de una forma estadísticamente significativa. Conclusiones: El cálculo de ClCr en el entorno de UCI proporciona datos fiables del FG, no siendo adecuado el uso de ecuaciones estimativas.(AU)

Background and objective: There is a growing body of evidence that the equations used to estimate the glomerular filtration rate (GFR) are not suitable in critically ill patients, a population whose GFR fluctuates continuously. Glomerular filtration is usually estimated by measuring urine creatinine clearance (CrCl) at various time points. The aim of our study was to evaluate the performance of the most widely used GFR calculators in the subpopulation of critically ill patients admitted for severe trauma, and to compare the results against determinations of CrCl in urine collected over a 4-hour period (4h-CrCl). Material and methods: Observational study in patients hospitalized for severe trauma. We measured the 4h-CrCl and estimated GFR using the Cockcroft-Gault, modified Jelliffe, MDRD, t-MDRD, and CKD-EPI equations, adjusting the results for body surface area (BSA) (ml/min/1.73m2). Data were analysed using R version 4.0.4. Results: A total of 85 patients were included. Median age was 51years, and 68 were men (78.82%). The mean BSA-adjusted 4h-CrCl (4h-ClCr/1.73m2) was 84.5ml/min/1.73m2. We found that GFR estimated using the t-MDRD equation correlated significantly with 4h-CrCl/1.73m2. The Cockcroft-Gault equation correlated significantly with 4h-CrCl/1.73m2 when GFR was greater than 130ml/min/m2. Conclusions: In ICU patients, glomerular filtration can be reliably estimated by determining urine CrCl, but GFR calculators are not accurate in this population.(AU)

Concordance between glomerular filtration rate estimation equations and 4-hour urinary creatinine clearance in critically ill patients with severe trauma.

BACKGROUND AND OBJECTIVE: There is a growing body of evidence that the equations used to estimate the glomerular filtration rate (GFR) are not suitable in critically ill patients, a population whose GFR fluctuates continuously. Glomerular filtration is usually estimated by measuring urine creatinine clearance (CrCl) at various time points. The aim of our study was to evaluate the performance of the most widely used GFR calculators in the subpopulation of critically ill patients admitted for severe trauma, and to compare the results against determinations of CrCl in urine collected over a 4-h period (4h-CrCl). MATERIAL AND METHODS: Observational study in patients hospitalized for severe trauma. We measured the 4h-CrCl and estimated GFR using the Cockcroft-Gault, modified Jelliffe, MDRD, t-MDRD, and CKD-EPI equations, adjusting the results for body surface area (BSA) (ml/min/1.73m2). Data were analysed using R version 4.0.4. RESULTS: A total of 85 patients were included. Median age was 51 years, and 68 were men (78.82%). The mean BSA-adjusted 4h-CrCl (4h-ClCr/1.73m2) was 84.5 ml/min/1.73m2. We found that GFR estimated using the t-MDRD equation correlated significantly with 4h-CrCl/1.73m2. The Cockcroft-Gault equation correlated significantly with 4h-CrCl/1.73m2 when GFR was greater than 130ml/min/m2. CONCLUSIONS: In ICU patients, glomerular filtration can be reliably estimated by determining urine CrCl, but GFR calculators are not accurate in this population.

Posterior reversible encephalopathy syndrome in critical COVID-19 patients: Report of 2 cases.

Posterior reversible encephalopathy syndrome is an acute neurological disorder characterized by variable symptoms and radiological images characteristic of vasogenic parietal-occipital edema. It is associated with clinical conditions such as high blood pressure, infection/sepsis, or cytotoxic/immunosuppressive drugs, among others. It is characterized pathophysiologically by endothelial damage with breakdown of blood-brain barrier, cerebral hypoperfusion, and vasogenic edema. The cases are presented on 2 critical COVID-19 patients who were admitted to pneumonia requiring mechanical ventilation and who, after removing sedation, developed acute and reversible neurological symptoms consisting of epilepsy and encephalopathy, associated with hyperintense subcortical lesions on brain magnetic resonance imaging compatible with posterior reversible encephalopathy syndrome. SARS-CoV-2 coronavirus would activate an inflammatory response that would damage brain endothelium. It could be triggered by cytokine release, as well as by direct viral injury, given that endothelium expresses ACE2 receptors. It could explain the possible association between posterior reversible encephalopathy syndrome and COVID-19.

Síndrome de encefalopatía posterior reversible en pacientes críticos COVID-19: reporte de 2 casos / Posterior reversible encephalopathy syndrome in critical COVID-19 patients: Report of 2 cases

El síndrome de encefalopatía posterior reversible es un trastorno neurológico agudo caracterizado por una sintomatología variable e imágenes radiológicas características de edema vasogénico parietooccipital. Está asociado a condiciones clínicas como hipertensión arterial, infección/sepsis o fármacos citotóxicos/inmunosupresores, entre otros. Se caracteriza fisiopatológicamente por daño endotelial con rotura de la barrera hematoencefálica, hipoperfusión cerebral y edema vasogénico. Presentamos 2 casos de pacientes críticos COVID-19 que ingresaron por neumonía con necesidad de ventilación mecánica y que tras retirar la sedación desarrollaron clínica neurológica aguda y reversible consistente en epilepsia y encefalopatía, asociada a lesiones subcorticales hiperintensas en la resonancia magnética cerebral compatibles con síndrome de encefalopatía posterior reversible. El coronavirus SARS-CoV-2 activaría una respuesta inflamatoria que produciría daño en el endotelio cerebral. Este último podría ser desencadenado por la liberación de citocinas, así como por una lesión viral directa, dado que el endotelio expresa receptores ACE2. Esto podría explicar la posible asociación entre el síndrome de encefalopatía posterior reversible y la COVID-19.(AU)

Posterior reversible encephalopathy syndrome is an acute neurological disorder characterized by variable symptoms and radiological images characteristic of vasogenic parietal-occipital edema. It is associated with clinical conditions such as high blood pressure, infection/sepsis, or cytotoxic/immunosuppressive drugs, among others. It is characterized pathophysiologically by endothelial damage with breakdown of blood-brain barrier, cerebral hypoperfusion, and vasogenic edema. The cases are presented on 2 critical COVID-19 patients who were admitted to pneumonia requiring mechanical ventilation and who, after removing sedation, developed acute and reversible neurological symptoms consisting of epilepsy and encephalopathy, associated with hyperintense subcortical lesions on brain magnetic resonance imaging compatible with posterior reversible encephalopathy syndrome. SARS-CoV-2 coronavirus would activate an inflammatory response that would damage brain endothelium. It could be triggered by cytokine release, as well as by direct viral injury, given that endothelium expresses ACE2 receptors. It could explain the possible association between posterior reversible encephalopathy syndrome and COVID-19.(AU)

[Posterior reversible encephalopathy syndrome in critical COVID-19 patients: Report of 2 cases]. / Síndrome de encefalopatía posterior reversible en pacientes críticos COVID-19: reporte de 2 casos.

Posterior reversible encephalopathy syndrome is an acute neurological disorder characterized by variable symptoms and radiological images characteristic of vasogenic parietal-occipital edema. It is associated with clinical conditions such as high blood pressure, infection/sepsis, or cytotoxic/immunosuppressive drugs, among others. It is characterized pathophysiologically by endothelial damage with breakdown of blood-brain barrier, cerebral hypoperfusion, and vasogenic edema.The cases are presented on 2 critical COVID-19 patients who were admitted to pneumonia requiring mechanical ventilation and who, after removing sedation, developed acute and reversible neurological symptoms consisting of epilepsy and encephalopathy, associated with hyperintense subcortical lesions on brain magnetic resonance imaging compatible with posterior reversible encephalopathy syndrome.SARS-CoV-2 coronavirus would activate an inflammatory response that would damage brain endothelium. It could be triggered by cytokine release, as well as by direct viral injury, given that endothelium expresses ACE2 receptors. It could explain the possible association between posterior reversible encephalopathy syndrome and COVID-19.