ABSTRACT
Acute Kidney Injury (AKI) complicating major trauma is associated with increased mortality and morbidity. Traumatic AKI has specific risk factors and predictable time-course facilitating diagnostic modelling. In a single centre, retrospective observational study we developed risk prediction models for AKI after trauma based on data around intensive care admission. Models predicting AKI were developed using data from 830 patients, using data reduction followed by logistic regression, and were independently validated in a further 564 patients. AKI occurred in 163/830 (19.6%) with 42 (5.1%) receiving renal replacement therapy (RRT). First serum creatinine and phosphate, units of blood transfused in first 24 h, age and Charlson score discriminated need for RRT and AKI early after trauma. For RRT c-statistics were good to excellent: development: 0.92 (0.88-0.96), validation: 0.91 (0.86-0.97). Modelling AKI stage 2-3, c-statistics were also good, development: 0.81 (0.75-0.88) and validation: 0.83 (0.74-0.92). The model predicting AKI stage 1-3 performed moderately, development: c-statistic 0.77 (0.72-0.81), validation: 0.70 (0.64-0.77). Despite good discrimination of need for RRT, positive predictive values (PPV) at the optimal cut-off were only 23.0% (13.7-42.7) in development. However, PPV for the alternative endpoint of RRT and/or death improved to 41.2% (34.8-48.1) highlighting death as a clinically relevant endpoint to RRT.
Subject(s)
Acute Kidney Injury/diagnosis , Acute Kidney Injury/etiology , Wounds and Injuries/complications , Acute Kidney Injury/surgery , Adult , Cohort Studies , Critical Care , Female , Humans , Incidence , Intensive Care Units/statistics & numerical data , Logistic Models , Male , Middle Aged , Renal Replacement Therapy , Retrospective Studies , Risk FactorsABSTRACT
PURPOSE: The purpose of this study is to describe the effect of levosimendan (without loading dose) on hemodynamics, inotropes/vasopressors, and mortality in acute heart failure (AHF). MATERIALS AND METHODS: Patients who received levosimendan for AHF were analyzed. Levosimendan dose, hemodynamic data, inotrope/vasopressor requirements, and fluid balance before commencement, at conclusion of, and 24 hours after levosimendan were collected. Mortality is also reported. RESULTS: Eighty-seven patients were analyzed. The mean levosimendan dose (without loading) was 0.096 µg/kg per minute (±0.014), and mean duration, 26 (±7.2) hours. There was no change in heart rate (start, post, and 24 hours post) (92 [±19], 92 [±26], and 92 [±15]) or mean arterial pressure (69 [±10], 72 [±8], and 72 [±10] mm Hg, respectively). There was a significant reduction in median dobutamine from 7.27 to 0 µg/kg per minute and noradrenaline from 0.20 to 0.1 µg/kg per minute before and 24 hours after. There was a significant increase in both mean cardiac index from 2.38 ± 0.0.72 to 2.98 ± 0.0.77 L/min per square meter and in markers of perfusion: base excess from -2.77 to 0.39 mmol/L, and lactate from 2.1 to 1.4 mmol/L before and 24 hours after infusion. Survival was 53%. CONCLUSIONS: Levosimendan, without a loading dose, improved cardiac index and perfusion while allowing a reduction in inotropic/vasopressor requirements in patients with AHF.
