Physiological and self-assessed psychological stress induced by a high fidelity simulation course among third year anesthesia and critical care residents: An observational study.

INTRODUCTION: The use of high fidelity simulators in Medicine can improve knowledge, behaviour and practice but may be associated with significant stress. Our objective was to measure physiological and psychological self-assessed intensity of stress before and after a planned simulation training session among third year anaesthesia and critical care residents. METHODS: A convenience sample of 27 residents participating in a simulation training course was studied. Stress was evaluated by self-assessment using a numerical scale and by salivary amylase concentration before and after the session. Technical and non-technical (using the Aberdeen Anaesthetists' Non Technical Skills scale) performances were assessed through videotapes analysis. RESULTS: The median stress score was 5 (2-8) before and 7 (2-10) after the simulation session (P<0.001). For 48% of residents studied, the stress score after the session was superior or equal to 8/10. Salivary amylase concentration increased significantly after the session compared to before the session, respectively (1,250,440±1,216,667 vs. 727,260±603,787IU/L, P=0.008). There was no significant correlation between stress parameters and non-technical performance. DISCUSSION: Simulation-induced stress, as measured by self-assessment and biological parameter, is high before the session and increases significantly during the course. While this stress did not seem to impact performance negatively, it should be taken into account.

Should kidney tubular markers be adjusted for urine creatinine? The example of urinary cystatin C.

BACKGROUND: Evaluation of specific urinary markers with respect to urine creatinine (uCreat) is common. However, as uCreat is a function of both glomerular filtration and tubular secretion, using uCreat for specific tubular markers, suggests that glomerular function is normal, and there is no tubular secretion. Thus, adjusting values of any tubular marker to uCreat, especially in patients with acute or even moderate chronic renal failure, can be misleading. METHODS: Using urine cystatin-C (uCST3) as a model tubular marker for following 120 kidney graft recipients daily, we evaluated the utility of either uCST3 alone or the uCST3/uCreat ratio to detect tubular damage. All positive kidney biopsies were always associated with a uCST3>0.18 mg/L. RESULTS: Using the uCST3/uCreat ratio, discrepancies regarding biopsy status were observed in nine patients (4 false positive, 5 false negative results). In two patients, variability of uCreat appeared to be the most important factor causing inconsistent uCST3/uCreat ratios. With a negative predictive value (NPV) of 85.7%, uCST3/uCreat can lead to errors in clinical interpretation. These errors can be avoided when estimates of tubular damage are based on uCST3 concentrations alone (NPV=100%). CONCLUSIONS: We recommend using the uCST3 value to evaluate the extent of renal tubular damage. Indeed, our conflicting results on uCST3/uCreat can be extended to every marker of tubular function. Evaluating a urine marker specific for renal tubular damage to a second urine marker that is itself strongly dependent upon glomerular or other renal or non-renal conditions, impairs its clinical relevance and may lead to incorrect interpretations. Correction with uCreat can be performed only in pure glomerulopathy, when specific markers of glomerular function are measured (i.e., urinary albumin). In all other cases of renal diseases, such correction is inappropriate and should be avoided. Clin Chem Lab Med 2009;47:1553-6.

Urinary cystatin C as a specific marker of tubular dysfunction.

BACKGROUND: Cystatin C (CST3), a strong inhibitor of cysteine proteinases, is freely filtered by the kidney glomerulus and is reabsorbed by the tubules, where it is almost totally catabolized, with the remainder then eliminated in urine. In tubular diseases, it seems sensible to postulate that CST3 degradation would be reduced and consequently an increase in its urinary elimination would be observed. METHODS: We report here the development of an automatic quantitative assay to measure CST3 concentrations in urine using a Behring N-Latex Cystatin C kit on a BNII laser nephelometer. We tested its clinical relevance on several kidney disease patients. RESULTS: This assay is sensitive (limit of detection 0.008 mg/L) and precise (within- and between-day CVs < 4%). Reference values for freshly collected urine samples range from 0.03 to 0.18 mg/L. Mean urine CST3 concentrations obtained from 52 patients with kidney tubular disease (4.31 +/- 3.85 mg/L) were significantly higher than those for 60 controls (0.096 +/- 0.044 mg/L; p < 0.0001) and 47 glomerular disease patients (0.106 +/- 0.133 mg/L; p < 0.0001). CONCLUSION: Increased urinary CST3 concentrations allow the accurate detection of tubular dysfunction among pure and mixed nephropathies. Because of its ability to be processed on automated clinical chemistry analyzers, this assay could easily be used as an adjunct to the standard panel used to screen kidney pathologies, even in emergency situations.