Pilot study comparing simulation-based and didactic lecture-based critical care teaching for final-year medical students.

BACKGROUND: Simulation-based medical education has rapidly evolved over the past two decades, despite this, there are few published reports of its use in critical care teaching. We hypothesised that simulation-based teaching of a critical care topic to final-year medical students is superior to lecture-based teaching. METHODS: Thirty-nine final-year medical students were randomly assigned to either simulation-based or lecture-based teaching in the chosen critical care topic. The study was conducted over a 6-week period. Efficacy of each teaching method was compared through use of multiple choice questionnaires (MCQ) - baseline, post-teaching and 2 week follow-up. Student satisfaction was evaluated by means of a questionnaire. Feasibility and resource requirements were documented by teachers. RESULTS: Eighteen students were randomised to simulation-based, and 21 to lecture-based teaching. There were no differences in age and gender between groups (p > 0.05). Simulation proved more resource intensive requiring specialised equipment, two instructors, and increased duration of teaching sessions (126.7 min (SD = 4.71) vs 68.3 min (SD = 2.36)). Students ranked simulation-based teaching higher with regard to enjoyment (p = 0.0044), interest (p = 0.0068), relevance to taught subject (p = 0.0313), ease of understanding (p = 0.0476) and accessibility to posing questions (p = 0.001). Both groups demonstrated improvement in post-teaching MCQ from baseline (p = 0.0002), with greater improvement seen among the simulation group (p = 0.0387), however, baseline scores were higher among the lecture group. The results of the 2-week follow-up MCQ and post-teaching MCQ were not statistically significant when each modality were compared. DISCUSSION: Simulation was perceived as more enjoyable by students. Although there was a greater improvement in post-teaching MCQ among the simulator group, baseline scores were higher among lecture group which limits interpretation of efficacy. Simulation is more resource intensive, as demonstrated by increased duration and personnel required, and this may have affected our results. CONCLUSIONS: The current pilot may be of use in informing future studies in this area.

Sepsis protects the myocardium and other organs from subsequent ischaemic/reperfusion injury via a MAPK-dependent mechanism.

BACKGROUND: Sepsis has been shown to precondition the intact heart against ischaemia/reperfusion (IR) injury, and prior endotoxin exposure of cells in in vitro models has shown evidence of protection against subsequent simulated ischaemia. Our aim in this study is to validate these findings and further investigate the signaling pathways involved. METHODS: Adult male Sprague Dawley rats were randomised to control (n = 7) or caecal ligation and perforation (CLP)-induced sepsis (n = 7). Hearts were harvested at 48 h, suspended in Langendorff mode and subjected to 30-min global ischaemia followed by 90-min reperfusion. In subsequent experiments, designed to determine the mechanisms by which sepsis protected against ischaemic injury, endotoxin-stimulated isolated cardiomyocytes, pulmonary A549 cells and renal HK2 cells were subjected to normoxic and hypoxic conditions. The roles of key pathways, including mitogen-activated protein (MAP) kinases extracellular-regulated protein kinase (ERK) 1/2, p38 MAPK (p38), c-Jun NH2-terminal protein kinase (JNK)), and nuclear factor-kappaB (NF-κB) were examined. RESULTS: Systemic sepsis protected isolated hearts from subsequent ischaemic/reperfusion-induced injury, enhancing functional recovery on reperfusion [developed left ventricular pressure ((d)LVP) mean(SE) 66.63(±10.7) mmHg vs. 54.13(±9.9) mmHg; LVPmax at 60 min 67.29(±11.9) vs. 72.48(±9.3), sepsis vs. control] despite significantly reduced baseline LV function in CLP animals (p < 0.001). Septic preconditioning significantly reduced infarct size after IR injury (p < 0.05). Endotoxin exposure protected isolated cardiomyocytes against hypoxia-induced cell death (p < 0.001). This effect appeared mediated in part via the p38, JNK and NF-κB pathways, but was independent of the ERK pathway, and did not appear to be mediated via HMGB1. The preconditioning effect of endotoxin was also demonstrated in isolated kidney and lung cells, suggesting that this preconditioning effect of sepsis is not confined to the myocardium. CONCLUSIONS: Sepsis preconditions the isolated rat heart against myocardial IR injury. These effects appeared to be mediated in part via the p38, JNK and NF-κB and pathways, but were independent of the ERK and HMGB pathways.

Urinary glutathione S-transferase as an early marker for renal dysfunction in patients admitted to intensive care with sepsis.

OBJECTIVE: Diagnosis of acute kidney injury (AKI) relies on measurement of serum creatinine concentration and urine flow, which change slowly and have low specificity and sensitivity. We investigated the potential of urinary levels of alpha-glutathione S-transferase (alpha-GST) and pi-GST - markers of proximal and distal renal tubule damage, respectively - to provide an earlier and more accurate indication of AKI in patients in the intensive care unit. DESIGN, SETTING AND PARTICIPANTS: Urine samples were collected over the 48 hours after ICU admission from 40 consecutive patients who were admitted with a diagnosis of sepsis between October 2007 and May 2008. AKI was diagnosed during the 48h after ICU admission with the criteria of the Acute Kidney Injury Network (AKIN). Urinary alpha-GST and pi-GST levels were measured with commercially available enzyme-linked immunosorbent assay (ELISA) kits. Serum creatinine concentration was also measured. Haemodynamic and resuscitation parameters were recorded, but managed independently by the ICU team. RESULTS: Urine samples were analysed from 38 patients (21 men, 17 women) with a median age of 54 years (interquartile range [IQR], 41-69 years), median APACHE II score of 13.3 (IQR, 8-17), and median ICU length of stay of 9 days (IQR, 3-19 days). Hospital mortality was 24%, and ICU mortality was 13%. Nineteen patients (50%) developed AKI, all within 24h of ICU admission. Urinary alpha-GST level was not increased in patients who developed AKI versus non-AKI patients. Median (IQR) urinary pi-GST level (microg/L) at ICU admission was 10.8 (4.7-22.65) in the non-AKI group, 19.3 (2.88-44) in those who developed Stage 1 AKI, and 27.4 (14.8-43.8) in those who developed Stage 3 AKI. Median urinary pi-GST level at ICU admission was higher in all groups than in healthy control subjects. The area under the receiver operating characteristics curve for urinary pi-GST level indicated that it was not a good predictor of AKI. CONCLUSIONS: Urinary pi-GST is elevated early in all patients with sepsis syndrome, but is not predictive of AKI as defined by AKIN. This may indicate sensitive detection of an earlier phase of kidney injury, and suggests that sepsis-related renal injury affects the distal tubules, giving new insights into the pathophysiology of AKI in sepsis.

Cerebral fat embolism syndrome causing brain death after long-bone fractures and acetazolamide therapy.

A 19-year-old woman with multiple fractures and mild brain injury developed severe cerebral fat embolism syndrome after "damage control" orthopaedic surgery. Acetazolamide therapy to manage ocular trauma, in association with hyperchloraemia, caused a profound metabolic acidosis with appropriate compensatory hypocapnia. During ventilator weaning, unexpected brainstem coning followed increased sedation and brief normalisation of arterial carbon dioxide concentration. Autopsy found severe cerebral fat embolism and brain oedema. In patients with multiple trauma, cerebral fat embolism syndrome is difficult to diagnose, and may be more common after delayed fixation of long-bone fractures. Acetazolamide should be used with caution, as sudden restoration of normocapnia during compensated metabolic acidosis in patients with raised intracranial pressure may precipitate coning.