Echocardiography for Intraoperative Decision Making in Mitral Valve Surgery-A Pilot Simulation-Based Training Module.

Echocardiographic assessment of the repaired or replaced mitral valve intraoperatively involves making a high-impact joint decision with the surgeon, in a time-sensitive manner, in a dynamic clinical situation. These decisions have to take into account the degree of imperfection if any, the likelihood of obtaining a better result, the underlying condition of the patient, and the impact of a longer cardiopulmonary bypass period if the decision is made to reintervene. Traditional echocardiography teaching is limited in its ability to provide this training. The authors report the development and implementation of a training module simulating the dynamic clinical environment of a mitral valve surgery in progress and the critical echo-based intraoperative decision making involved in the assessment of the acceptability of the surgical result.

Comparison of virtual patient simulation with mannequin-based simulation for improving clinical performances in assessing and managing clinical deterioration: randomized controlled trial.

BACKGROUND: Virtual patient simulation has grown substantially in health care education. A virtual patient simulation was developed as a refresher training course to reinforce nursing clinical performance in assessing and managing deteriorating patients. OBJECTIVE: The objective of this study was to describe the development of the virtual patient simulation and evaluate its efficacy, by comparing with a conventional mannequin-based simulation, for improving the nursing students' performances in assessing and managing patients with clinical deterioration. METHODS: A randomized controlled study was conducted with 57 third-year nursing students who were recruited through email. After a baseline evaluation of all participants' clinical performance in a simulated environment, the experimental group received a 2-hour fully automated virtual patient simulation while the control group received 2-hour facilitator-led mannequin-based simulation training. All participants were then re-tested one day (first posttest) and 2.5 months (second posttest) after the intervention. The participants from the experimental group completed a survey to evaluate their learning experiences with the newly developed virtual patient simulation. RESULTS: Compared to their baseline scores, both experimental and control groups demonstrated significant improvements (P<.001) in first and second post-test scores. While the experimental group had significantly lower (P<.05) second post-test scores compared with the first post-test scores, no significant difference (P=.94) was found between these two scores for the control group. The scores between groups did not differ significantly over time (P=.17). The virtual patient simulation was rated positively. CONCLUSIONS: A virtual patient simulation for a refreshing training course on assessing and managing clinical deterioration was developed. Although the randomized controlled study did not show that the virtual patient simulation was superior to mannequin-based simulation, both simulations have demonstrated to be effective refresher learning strategies for improving nursing students' clinical performance. Given the greater resource requirements of mannequin-based simulation, the virtual patient simulation provides a more promising alternative learning strategy to mitigate the decay of clinical performance over time.

Interprofessional simulation-based education program: a promising approach for changing stereotypes and improving attitudes toward nurse-physician collaboration.

An effective working relationship between physicians and nurses is enhanced by fostering positive perceptions and collaborative attitudes between the two professions. This brief paper examines the effect of an interprofessional simulation-based communication education program in enhancing medical and nursing students' perceptions of each other's profession and their attitudes toward nurse-physician collaboration. Pretest-Posttest design was conducted on 96 medical and nursing students who demonstrated the existence of professional stereotypes in the baseline data. This study showed that by promoting open communication, shared information and decision-making, mutual respect, and trust during the interprofessional simulation training, a positive transformation on the stereotypes and attitudes toward nurse-physician collaboration can be achieved.

Terminal arbor degeneration--a novel lesion produced by the antineoplastic agent paclitaxel.

The antineoplastic agent paclitaxel causes a dose-limiting distal, symmetrical, sensory peripheral neuropathy that is often accompanied by a neuropathic pain syndrome. In a low-dose model of paclitaxel-evoked painful peripheral neuropathy in the rat, we have shown that the drug causes degeneration of intraepidermal nerve fibers (IENFs), i.e. the fibers which give rise to the sensory afferent's terminal receptor arbor. However, we did not find any evidence for axonal degeneration in samples taken at the mid-nerve level. Here we aimed to determine whether the absence of degenerating peripheral nerve axons was due to sampling a level that was too proximal. We used electron microscopy to study the distal-most branches of the nerves innervating the hind paw glabrous skin of normal and paclitaxel-treated rats. We confirmed that we sampled at a time when IENF degeneration was prominent. Because degeneration might be easier to detect with higher paclitaxel doses, we examined a four-fold cumulative dose range (8-32 mg/kg). We found no evidence of degeneration in the superficial subepidermal axon bundles (sSAB) that are located just a few microns below the epidermal basal lamina. Specifically, for all three dose groups there was no change in the number of sSAB per millimeter of epidermal border, no change in the number of axons per sSAB and no change in the diameter of sSAB axons. We conclude that paclitaxel produces a novel type of lesion that is restricted to the afferent axon's terminal arbor; we name this lesion 'terminal arbor degeneration'.

Cutaneous tactile allodynia associated with microvascular dysfunction in muscle.

BACKGROUND: Cutaneous tactile allodynia, or painful hypersensitivity to mechanical stimulation of the skin, is typically associated with neuropathic pain, although also present in chronic pain patients who do not have evidence of nerve injury. We examine whether deep tissue microvascular dysfunction, a feature common in chronic non-neuropathic pain, contributes to allodynia. RESULTS: Persistent cutaneous allodynia is produced in rats following a hind paw ischemia-reperfusion injury that induces microvascular dysfunction, including arterial vasospasms and capillary slow flow/no-reflow, in muscle. Microvascular dysfunction leads to persistent muscle ischemia, a reduction of intraepidermal nerve fibers, and allodynia correlated with muscle ischemia, but not with skin nerve loss. The affected hind paw muscle shows lipid peroxidation, an upregulation of nuclear factor kappa B, and enhanced pro-inflammatory cytokines, while allodynia is relieved by agents that inhibit these alterations. Allodynia is increased, along with hind paw muscle lactate, when these rats exercise, and is reduced by an acid sensing ion channel antagonist. CONCLUSION: Our results demonstrate how microvascular dysfunction and ischemia in muscle can play a critical role in the development of cutaneous allodynia, and encourage the study of how these mechanisms contribute to chronic pain. We anticipate that focus on the pain mechanisms associated with microvascular dysfunction in muscle will provide new effective treatments for chronic pain patients with cutaneous tactile allodynia.

Levels of neuropeptides nocistatin, nociceptin/orphanin FQ and their precursor protein in a rat neuropathic pain model.

Neuropeptides nociceptin/orphanin FQ (N/OFQ) and nocistatin (NST) are related to pain modulation. The amounts of these peptides and their precursor protein, prepronociceptin (ppN/OFQ) in the brain, spinal cord and serum samples of rats with partial sciatic nerve ligation (PSNL) were compared with those in naïve rats using radioimmunoassay (RIA). There was a significant rise in the levels of ppN/OFQ, N/OFQ and NST in the brains of PSNL rats. Their spinal cords showed significantly increased ppN/OFQ and NST levels but no change in N/OFQ levels. The PSNL rats also had increased serum NST (statistically significant) and N/OFQ (statistically insignificant) with decreased ppN/OFQ suggesting important roles of these peptides in neuropathic pain mechanism.

Dysregulation of cellular calcium homeostasis in chemotherapy-evoked painful peripheral neuropathy.

Paclitaxel and vincristine are chemotherapeutic drugs that often evoke a long-lasting painful peripheral neuropathy. Using drugs that reduce intracellular or extracellular calcium ions (Ca2+), we investigated the hypothesis that impaired Ca2+ regulation contributes to the chemotherapy-evoked neuropathic pain syndrome. For comparison, we also tested rats with painful peripheral neuropathy caused by nerve trauma and to the anti-human immunodeficiency virus nucleoside analog 2',3'-dideoxycytidine (ddC). Normal naïve (without neuropathy), paclitaxel-treated, and vincristine-treated rats received the following intrathecal injections: TMB-8 (46 nmol), Quin-2 (1.8 nmol), EGTA (0.1 micromol), EGTA-am (0.1 micromol), and their vehicle controls. Chronic constriction injury (CCI) rats were examined after TMB-8 and Quin-2 injections, and ddC-treated rats were examined after receiving TMB-8. Mechano-allodynia and mechano-hyperalgesia were evaluated after each injection. Drug effects on heat hyperalgesia were also tested in CCI rats. All four Ca2+-reducing drugs significantly inhibited mechano-allodynia and mechano-hyperalgesia in the rats treated with paclitaxel, vincristine, or ddC, but no effects were seen in the CCI or naïve rats. We conclude that a similar abnormality of cellular Ca2+ homeostasis contributes to the pain caused by paclitaxel, vincristine, and ddC, but not posttraumatic painful peripheral neuropathy.

Strengthening the afferent limb of rapid response systems: an educational intervention using web-based learning for early recognition and responding to deteriorating patients.

BACKGROUND: The timely recognition and response to patients with clinical deteriorations constitute the afferent limb failure of a rapid response system (RRS). This area is a persistent problem in acute healthcare settings worldwide. In this study, we evaluated the effect of an educational programme on improving the nurses' knowledge and performances in recognising and responding to clinical deterioration. METHOD: The interactive web-based programme addressed three areas: (1) early detection of changes in vital signs; (2) performance of nursing assessment and interventions using airway, breathing, circulation, disability and expose/examine and (3) reporting clinical deterioration using identity, situation, background, assessment and recommendation. Sixty-seven registered nurses participated in the randomised control study. The experimental group underwent a 3 h programme while the control group received no intervention. Pretests and post-tests, a mannequin-based assessment and a multiple-choice knowledge questionnaire were conducted. We evaluated the participants' performances in assessing, managing and reporting the deterioration of a patient using a validated performance tool. RESULTS: A significantly higher number of nurses from the experimental group than the control group monitored respiratory rates (48.2% vs 25%, p<0.05) and pulse rates (74.3% vs 37.5%, p<0.01) in the simulated environment, after the intervention. The post-test mean scores of the experimental group was significantly higher than the control group for knowledge (21.29 vs 18.28, p<0.001), performance in assessing and managing clinical deterioration (25.83 vs 19.50, p<0.001) and reporting clinical deterioration (12.83 vs 10.97, p<0.001). CONCLUSIONS: A web-based educational programme developed for hospital nurses to strengthen the afferent limb of the RRS significantly increased their knowledge and performances in assessing, managing and reporting clinical deterioration.

Characterization of a model of cutaneous inflammatory pain produced by an ultraviolet irradiation-evoked sterile injury in the rat.

Neuroimmune interactions are of known importance in the genesis and maintenance of inflammatory pain states. However, the immune response to tissue damage is likely to differ depending on whether or not the injury is accompanied by infection. Many clinically important inflammatory pain states involve a sterile tissue injury. However, existing animal models of cutaneous inflammatory pain use injuries that are likely to involve those components of the immune system that are specialized for combating pathogens (e.g., injections of Complete Freund's Adjuvant, carrageenan, or zymosan). We describe here a model of cutaneous inflammatory pain in the rat produced by a sterile injury evoked by a single exposure to ultraviolet irradiation. The animals develop heat-hyperalgesia, mechano-hyperalgesia, mechano-allodynia, and cold-allodynia that last for several days. Cold-allodynia appears within 6 h or less, but the other symptoms are not clearly evident until 12-36 h after exposure. This model offers several advantages for the experimental analysis of the causes of inflammatory allodynia and hyperalgesia.

An interprofessional communication training using simulation to enhance safe care for a deteriorating patient.

BACKGROUND: Communication and teamwork between doctors and nurses are critical for optimal patient care. Simulation and interprofessional team learning are emerging as significant learning strategies to promote teamwork and communication between different health professionals. AIM: The aim of the study is to describe the development, implementation and evaluation of a simulation-based interprofessional educational (Sim-IPE) program, using a presage-process-product (3P) model, for improving medical and nursing students' communication skills in caring of a patient with physiological deterioration. METHOD: The program was conducted using full-scale simulation and communication strategies adapted from Team Strategies and Tools to Enhance Performance and Patient Safety (TeamSTEPPS). 127 medical and nursing students participated in a 3-hour small group interprofessional learning that incorporated simulation scenarios of deteriorating patients. Pre and post-tests were conducted to assess the students' self-confidence in interprofessional communication and perception in interprofessional learning. After the training, the students completed a satisfaction questionnaire. RESULTS: Both medicine and nursing groups demonstrated a significant improvement on post-test score from pre-test score for self-confidence (p<.0001) and perception (p<.0001) with no significant differences detected between the two groups. The participants were highly satisfied with their simulation learning. CONCLUSION: The Sim-IPE has better prepared the medical and nursing students in communicating with one another in providing safe care for deteriorating patient. In addition, it has improved their perception towards interprofessional learning. This pre-registration interprofessional education could prepare them for more comprehensive interprofessional team learning at post-registration level.

Paclitaxel- and vincristine-evoked painful peripheral neuropathies: loss of epidermal innervation and activation of Langerhans cells.

Experimental painful peripheral neuropathies produced by the chemotherapeutic drugs, paclitaxel and vincristine, are produced by relatively low doses that do not cause axonal degeneration in peripheral nerve. Using quantitative immunolabeling with the PGP9.5 antibody, we have investigated whether these painful neuropathies might be associated with degeneration that is confined to the region of the sensory fiber's receptor terminals in the skin. Because complete and partial nerve transections are known to cause an increase in PGP9.5 in epidermal Langerhans cells (LCs), we also examined whether this effect occurs in chemotherapy-treated animals. At the time of peak pain severity, rats with paclitaxel- and vincristine-evoked painful peripheral neuropathies had a significant decrease (24% and 44%, respectively) in the number of intraepidermal nerve fibers (IENF) in the hind paw glabrous skin and an increase (217% and 121%, respectively) in the number of PGP9.5-positive LCs, relative to control. However, neither loss of IENF nor an increase in PGP9.5-positive LCs was found in rats with a painful peripheral neuropathy evoked by the anti-HIV agent, 2',3'-dideoxycytidine. We also confirmed that there is a decrease in IENF and an increase in PGP9.5-positive LCs in rats with neuropathic pain following a partial nerve injury (CCI model) and in rats with a complete sciatic nerve transection. Partial degeneration of the intraepidermal innervation suggests mechanisms that might produce chemotherapy-evoked neuropathic pain, and activation of cutaneous LCs suggests possible neuroimmune interactions that might also have a role.