The impact of a dedicated training program for oral examiners at a medical school in Germany: a survey among participants from operative and non-operative disciplines

BACKGROUND: Oral examinations have been a crucial format in ancient and modern assessment to evaluate and guarantee quality of medical education and thereby to secure patient safety. To achieve a high level of quality in the oral part of the final examination of medical students, a training program for oral examiners at the Medical Faculty of Ulm (Germany) has been established since 2007. However, little is known about the attitude of the examiners in regard to the impact of this training program and of oral examinations as instruments to ensure patient safety. METHODS: All 367 academic clinicians from operative and non-operative disciplines, attending the one-day examiner training program at the University of Ulm between 2007 and 2012 have been asked to answer an online survey (EvaSys 5.0). Focus of the survey was to find out in which respect the examiners profited from the trainings, if the training effects were discipline-dependent, and to which degree the oral examinations could contribute to patient safety. Statistical analysis was performed using the t-test for independent samples. Results were considered statistically significant when p < 0.05. RESULTS: A total of 63 participants answered the survey, but in 4 cases the questionnaire was not fully completed (with single items missing). More than half of the study participants (n = 34/59; 58%) have experienced (at least sometimes or rarely) candidates that they deemed incompetent and perhaps even dangerous to the patients’ health who nevertheless passed the oral exam successfully. The majority of participants were convinced that oral examinations using concrete clinical cases could significantly contribute to patient safety, if grading is based on clear criteria and if examinations as well as grading are performed more critically. The impact of the training program was rated significantly stronger by surgeons than by non-surgeons in several categories. These categories included “strengths and weaknesses of oral examinations”, “reliability”, “validity”, “competence in grading”, “critical grading”, and “departmental improvements” concerning oral examinations. CONCLUSIONS: In respect to patient safety, it seems crucial to prevent incompetent candidates from passing the oral examination. The present study indicates the importance to continue and to develop our examiner trainings, with main emphasis on concrete clinical problems and a criteria-based critical grading system for oral examinations. Since the impact of the training was particularly high for colleagues from the operative disciplines, the training program should be offered especially in surgical departments

Pathophysiology of septic encephalopathy - an unsolved puzzle

The exact cellular and molecular mechanisms of sepsis-induced encephalopathy remain elusive. The breakdown of the blood-brain barrier (BBB) is considered a focal point in the development of sepsis-induced brain damage. Contributing factors for the compromise of the BBB include cytokines and chemokines, activation of the complement cascade, phagocyte-derived toxic mediators, and bacterial products. To date, we are far from fully understanding the neuropathology that develops as a secondary remote organ injury as a consequence of sepsis. However, recent studies suggest that bacterial proteins may readily cross the functional BBB and trigger an inflammatory response in the subarachnoid space, in absence of a bacterial invasion. A better understanding of the pathophysiological events leading to septic encephalopathy appears crucial to advance the clinical care for this vulnerable patient population

Sepsis-Induced Adipokine Change with regard to Insulin Resistance

Background. Assessment of white adipose tissue has changed in recent years, with WAT now being considered as an active endocrine organ, secreting a large number of bioactive mediators, so-called adipokines. Besides other functions, these adipokines are involved in inflammatory response thereby exhibiting predominantly proinflammatory or anti-inflammatory properties and contribute to insulin resistance. Methods. Comprehensive review of the literature of the role of adipokines relevant to critical care medicine using PubMed search. Results. Adiponectin—the prototype of an anti-inflammatory and insulin-sensitizing adipokine—is diminished in sepsis, while resistin—a protein with proinflammatory properties—is elevated. Plasminogen activator inhibitor-1, interleukin (IL)-1, IL-6, IL-8, and IL-10, and tumor-necrosis-factor-alpha mediate insulin resistance and are elevated in sepsis, while retinol-binding protein-4 concentrations are significantly reduced in sepsis. Chemerin displays potent anti-inflammatory and insulin-resistance properties, while monocyte chemotactic protein-1—increased in sepsis—contributes to macrophage infiltration in adipose tissue and insulin resistance. Conclusions. The expression of adipokines in humans is altered as well in obese as in septic patients with elevated levels of proinflammatory adipokines. Changes in adipokine levels in acute sepsis could contribute to insulin resistance. Consequently, in critically ill patients, these alterations underline a possible contribution of adipokines in the development of hyperglycemia

Adipose tissue: a neglected organ in the response to severe trauma?

Despite the manifold recent efforts to improve patient outcomes, trauma still is a clinical and socioeconomical issue of major relevance especially in younger people. The systemic immune reaction after severe injury is characterized by a strong pro- and anti-inflammatory response. Besides its functions as energy storage depot and organ-protective cushion, adipose tissue regulates vital processes via its secretion products. However, there is little awareness of the important role of adipose tissue in regulating the posttraumatic inflammatory response. In this review, we delineate the local and systemic role of adipose tissue in trauma and outline different aspects of adipose tissue as an immunologically active modifier of inflammation and as an immune target of injured remote organs after severe trauma

New Insights into the Role of Peroxisome Proliferator-Activated Receptors in Regulating the Inflammatory Response after Tissue Injury

Major trauma results in a strong inflammatory response in injured tissue. This posttraumatic hyperinflammation has been implied in the adverse events leading to a breakdown of host defense mechanisms and ultimately to delayed organ failure. Ligands to peroxisome proliferator-activated receptors (PPARs) have recently been identified as potent modulators of inflammation in various acute and chronic inflammatory conditions. The main mechanism of action mediated by ligand binding to PPARs is the inhibition of the nuclear transcription factor NF-κB, leading to downregulation of downstream gene transcription, such as for genes encoding proinflammatory cytokines. Pharmacological PPAR agonists exert strong anti-inflammatory properties in various animal models of tissue injury, including central nervous system trauma, ischemia/reperfusion injury, sepsis, and shock. In addition, PPAR agonists have been shown to induce wound healing process after tissue trauma. The present review was designed to provide an up-to-date overview on the current understanding of the role of PPARs in the pathophysiology of the inflammatory response after major trauma. Therapeutic options for using recombinant PPAR agonists as pharmacological agents in the management of posttraumatic inflammation will be discussed

Complement After Trauma: Suturing Innate and Adaptive Immunity

The overpowering effect of trauma on the immune system is undisputed. Severe trauma is characterized by systemic cytokine generation, activation and dysregulation of systemic inflammatory response complementopathy and coagulopathy, has been immensely instrumental in understanding the underlying mechanisms of the innate immune system during systemic inflammation. The compartmentalized functions of the innate and adaptive immune systems are being gradually recognized as an overlapping, interactive and dynamic system of responsive elements. Nonetheless the current knowledge of the complement cascade and its interaction with adaptive immune response mediators and cells, including T- and B-cells, is limited. In this review, we discuss what is known about the bridging effects of the complement system on the adaptive immune system and which unexplored areas could be crucial in understanding how the complement and adaptive immune systems interact following trauma

Challenge to the Intestinal Mucosa During Sepsis

Sepsis is a complex of life-threating organ dysfunction in critically ill patients, with a primary infectious cause or through secondary infection of damaged tissues. The systemic consequences of sepsis have been intensively examined and evidences of local alterations and repercussions in the intestinal mucosal compartment is gradually defining gut-associated changes during sepsis. In the present review, we focus on sepsis-induced dysfunction of the intestinal barrier, consisting of an increased permeability of the epithelial lining, which may facilitate bacterial translocation. We discuss disturbances in intestinal vascular tonus and perfusion and coagulopathies with respect to their proposed underlying molecular mechanisms. The consequences of enzymatic responses by pancreatic proteases, intestinal alkaline phosphatases, and several matrix metalloproteases are also described. We conclude our insight with a discussion on novel therapeutic interventions derived from crucial aspects of the gut mucosal dynamics during sepsis

The Interplay between Child Maltreatment and Stressful Life Events during Adulthood and Cardiovascular Problems—A Representative Study

Psychological stress is a major risk factor for cardiovascular diseases. While the relevance of early life stress, such as that which is due to child maltreatment (CM), is well known to impact individual stress responses in the long-term, and data on the interplay between CM and stressful events in adulthood on cardiovascular health are sparse. Here, we aimed to assess how stressful life events in adulthood are associated with cardiovascular health infarction in later life and whether this association is independent of CM. In a cross-sectional design, a probability sample of the German population above the age of 14 was drawn using different sampling steps. The final sample included 2510 persons (53.3% women, mean age: 48.4 years). Participants were asked about sociodemographic factors, adult life events, CM, and health conditions in adulthood. Results indicate that the number of experienced adverse life events in adulthood is associated with significantly increased odds for obesity (Odds Ration (OR)women = 1.6 [1.3; 2.0], ORmen = 1.4 [1.1; 1.9]), diabetes (ORwomen = 1.5 [1.1; 2.1], ORmen = 1.5 [1.1; 2.3]) and myocardial infarction (ORwomen = 2.1 [1.0; 4.3], ORmen = 1.8 [1.1; 2.8]). This association is not moderated by the experience of CM, which is associated with cardiovascular problems independently. Taken together, adult stressful life events and CM are significantly and independently associated with cardiovascular health in men and women in the German population in a dose-dependent manner. General practitioners, cardiologists and health policy-makers should be aware of this association between psychosocial stressors during childhood and adulthood and cardiovascular health

Molecular mechanisms of inflammation and tissue injury after major trauma-is complement the "bad guy"?

Trauma represents the leading cause of death among young people in industrialized countries. Recent clinical and experimental studies have brought increasing evidence for activation of the innate immune system in contributing to the pathogenesis of trauma-induced sequelae and adverse outcome. As the "first line of defense", the complement system represents a potent effector arm of innate immunity, and has been implicated in mediating the early posttraumatic inflammatory response. Despite its generic beneficial functions, including pathogen elimination and immediate response to danger signals, complement activation may exert detrimental effects after trauma, in terms of mounting an "innocent bystander" attack on host tissue. Posttraumatic ischemia/reperfusion injuries represent the classic entity of complement-mediated tissue damage, adding to the "antigenic load" by exacerbation of local and systemic inflammation and release of toxic mediators. These pathophysiological sequelae have been shown to sustain the systemic inflammatory response syndrome after major trauma, and can ultimately contribute to remote organ injury and death. Numerous experimental models have been designed in recent years with the aim of mimicking the inflammatory reaction after trauma and to allow the testing of new pharmacological approaches, including the emergent concept of site-targeted complement inhibition. The present review provides an overview on the current understanding of the cellular and molecular mechanisms of complement activation after major trauma, with an emphasis of emerging therapeutic concepts which may provide the rationale for a "bench-to-bedside" approach in the design of future pharmacological strategies