Six steps from head to hand: a simulator based transfer oriented psychological training to improve patient safety

The incidence of human errors in the field of medicine is high. Two strategies to increase patient safety are simulator training and crew resource management (CRM) seminars, psychological courses on human performance and error management. AIM: To establish a CRM course combining psychological training on human error with simulator training. METHODS: Evaluation of a new 1-day training approach targeting physicians, nurses, and paramedics. The course was divided into four modules focusing on situation awareness, task management, teamwork, and decision-making. Each of the modules was set up according to a new six-step approach. The course started with an introduction into good CRM behaviour and an instructor demonstration of a simulator scenario. The participants had to debrief the instructors regarding their human performance. Step 2 was a lecture about the psychological background, and the third step consisted of psychological exercises related to the topic of the module. A psychological exercise in a medical context (MiniSim) made up step 4, which involved a patient simulator. The last two steps were a simulator scenario and a debriefing, as in other simulator courses. A psychologist and a physician were the facilitators in all steps. Two pilot courses were evaluated. RESULTS: Seventeen evaluation questionnaires were received. All participants rated the course as good (10) and very good (7). The psychological exercises were highly valued (good, 5; very good, 11 participants). Thirteen participants agreed that the course content was related to their work. CONCLUSION: We established the first course curriculum combining psychological teaching with simulator training for healthcare professionals in emergency medicine. Similar concepts using the six-step approach can be applied to other medical specialties.     

An improved assay with 4-(2-thiazolylazo)-resorcinol for non-esterified fatty acids in biological fluids

A simple and rapid colorimetric assay for non-esterified fatty acids (NEFA) was developed employing extraction of samples with 0.1 mol/l glycine (pH 2.7) and methoxyethanol : butyl ether, and formation of a copper-fatty acid soap detected with 4-(2-thiazolylazo)-resorcinol. The method developed is sensitive enough to detect as little as 11 nmol/0.25 ml sample. Results are not affected by marked molar excesses of phospholipids, cholesterol, cholesterol esters, triglycerides, bilirubin, or lactate. Recovery of palmitate in the extract averages 94.2 +/- 3.2% (S.D.) and other long chain fatty acids are recovered equally. The copper-NEFA-indicator complex formed is stable. Extracted samples can be stored for as long as 2 weeks without appreciable changes in measured NEFA content. The method developed is suitable for both manual and semi-automated procedures for determining NEFA content in biological fluids.     

Renal-associated TLR2 mediates ischemia/reperfusion injury in the kidney

TLRs are conserved pattern recognition receptors that detect motifs of pathogens and host material released during injury. For unknown reasons, renal TLR2 mRNA is mainly expressed by tubular cells and is enhanced upon renal ischemia/reperfusion (I/R) injury. We evaluated the role of TLR2 in I/R injury using TLR2-/- and TLR2+/+ mice, TLR2 antisense oligonucleotides, and chimeric mice deficient in leukocyte or renal TLR2. Tubular cells needed TLR2 to produce significant cytokine and chemokine amounts upon ischemia in vitro. TLR2 played a proinflammatory and detrimental role in vivo after I/R injury, as reflected by a reduction in the amount of local cytokines and chemokines, leukocytes, and the level of renal injury and dysfunction in TLR2-/- mice compared with controls. Analysis of chimeric mice suggested that TLR2 expressed on renal parenchyma plays a crucial role in the induction of inflammation and injury. TLR2-antisense treatment protected mice from renal dysfunction, neutrophil influx, and tubular apoptosis after I/R injury compared with nonsense treatment. In summary, we identified renal-associated TLR2 as an important initiator of inflammatory responses leading to renal injury and dysfunction in I/R injury. These data imply that TLR2 blockade could provide a basis for therapeutic strategies to treat or prevent renal ischemic injury.     

Acquired von Willebrand syndrome: experience from 2 years in a single laboratory compared with data from the literature and an international registry

Acquired von Willebrand syndrome (avWS) has gained more attention during the last years. An International Registry has been compared with the literature. It could be shown that the data collected from 123 publications compared well with the data from the registry, albeit with differences in the number of patients suffering from lymphoproliferative diseases and cardiovascular disorders, that were more prominent in the registry and the group of miscellaneous conditions underrepresented in the registry. Our data are clearly different for the lymphoproliferative diseases with only four patients in 2 years. These patients usually suffer from severe bleeding complications together with low to very low factor VIII/von Willebrand factor (FVIII/vWF) concentrations and thus will not go undiagnosed. In contrast to this, patients with cardiovascular disorders usually bleed only during surgical procedures or catheter procedures. At that time they have increased vWF parameters. Because of this and because the acute bleeding is of limited duration and usually not life threatening, many of them are discharged without a proper diagnosis and are only rarely referred to a specialized diagnostic work-up thereafter. In conclusion, avWS, although not a frequent disease, is nevertheless clearly underdiagnosed. This should be addressed in future prospective studies.     

Usefulness of positron emission tomography in defining myocardial viability in patients referred for cardiac transplantation

Positron emission tomography imaging detected evidence of viability in 17 of 33 patients with evidence of infarction only on their thallium scans who were referred for transplant evaluation. Eleven of these 17 underwent revascularization with excellent outcome.     

p23, a major COPI-vesicle membrane protein, constitutively cycles through the early secretory pathway

A novel type I transmembrane protein of COPI-coated vesicles, p23, has been demonstrated to be localized mainly to the Golgi complex. This protein and p24, another member of the p24 family, have been shown to bind coatomer via their short cytoplasmic tails. Here we demonstrate that p23 continuously cycles through the early secretory pathway. The cytoplasmic tail of p23 is shown to act as a functional retrieval signal as it confers endoplasmic reticulum (ER) residence to a CD8–p23 fusion protein. This ER localization is, at least in part, a result of retrieval from post-ER compartments because CD8–p23 fusion proteins receive post-ER modifications. In contrast, the cytoplasmic tail of p24 has been shown not to retrieve a CD8–p24 fusion protein. The coatomer binding motifs FF and KK in the cytoplasmic tail of p23 are reported to influence the steady-state localization of the CD8–p23 fusion protein within the ER–Golgi recycling pathway. It appears that the steady-state Golgi localization of endogenous p23 is maintained by its lumenal domain, as a fusion protein with the lumenal domain of CD8, and the membrane span as well as the cytoplasmic tail of p23 is no longer detected in the Golgi.     

Compromise of beneficial effects of reperfusion on myocardium supplied by vessels with critical residual stenosis

Coronary thrombolysis in patients frequently unmasks high grade residual stenosis. To determine whether beneficial effects of reperfusion are compromised by critical residual coronary stenosis, 14 dogs were instrumented with an external left anterior descending coronary artery balloon occluder, Doppler flow probe and adjustable screw clamp. In eight of the dogs, critical stenosis (abolition of reactive hyperemia after a 20 s occlusion; 95.7 +/- 1.0% cross-sectional area reduction) was induced before occlusion and maintained. In the control group (n = 6), no stenosis was induced. Each dog was subjected to 2 h of myocardial ischemia followed by balloon deflation and 24 h of reperfusion. Myocardial blood flow assessed with microspheres was similar during balloon inflation in both groups and indicative of profound ischemia. Transmural blood flow to the reperfused zone assessed 1 min after balloon deflation was significantly greater in control dogs without residual stenosis (383% of normal compared with 120% of normal in dogs with stenosis) (p less than 0.01). Compromise of transmural flow persisted in dogs with stenosis (85% compared with 121% of normal in control dogs after 1 h, p less than 0.05; and 49% compared with 68% after 24 h of reperfusion, p less than 0.05). Diminution of subendocardial blood flow after reperfusion was particularly marked. The extent of infarction was greater in the heart of dogs with residual stenosis. Thus, residual critical coronary stenosis compromises nutritional perfusion and salvage of reperfused myocardium after recanalization. These observations underscore the need for prompt identification of patients with high grade residual stenosis early after coronary thrombolysis and the potential value of angioplasty or coronary surgery in selected patients soon after initial recanalization.