Search

In 2018, the American Board of Anesthesiology (ABA) became the first US medical specialty certifying board to incorporate an Objective Structured Clinical Examination (OSCE) into its initial certification examination system. Previously, the ABA's staged examination system consisted of 2 written examinations (the BASIC and ADVANCED examinations) and the Standardized Oral Examination (SOE). The OSCE and the existing SOE are now 2 separate components of the APPLIED Examination. This report presents the results of the first-year OSCE administration. A total of 1410 candidates took both the OSCE and the SOE in 2018. Candidate performance approximated a normal distribution for both the OSCE and the SOE, and was not associated with the timing of the examination, including day of the week, morning versus afternoon session, and order of the OSCE and the SOE. Practice-based Learning and Improvement was the most difficult station, while Application of Ultrasonography was the least difficult. The correlation coefficient between SOE and OSCE scores was 0.35 ([95% confidence interval {CI}, 0.30-0.39]; P < .001). Scores for the written ADVANCED Examination were modestly correlated with scores for the SOE (r = 0.29 [95% CI, 0.25-0.34]; P < .001) and the OSCE (r = 0.15 [95% CI, 0.10-0.20]; P < .001). Most of the candidates who failed the SOE passed the OSCE, and most of the candidates who failed the OSCE passed the SOE. Of the 1410 candidates, 77 (5.5%) failed the OSCE, 155 (11.0%) failed the SOE, and 25 (1.8%) failed both. Thus, 207 (14.7%) failed at least 1 component of the APPLIED Examination. Adding an OSCE to a board certification examination system is feasible. Preliminary evidence indicates that the OSCE measures aspects of candidate abilities distinct from those measured by other examinations used for initial board certification.

BACKGROUND Scholarly activity is expected of program directors of Accreditation Council for Graduate Medical Education (ACGME)-accredited residency training programs. Anesthesiology residency programs are cited more often than surgical programs for deficiencies in academic productivity. We hypothesized that this may in part reflect differences in scholarly activity between program directors of anesthesiology and surgical trainings programs. To test the hypothesis, we examined the career track record of current program directors of ACGME-accredited anesthesiology and surgical residency programs at the same institutions using PubMed citations and funding from the National Institutes of Health (NIH) as metrics of scholarly activity. METHODS Between November 1, 2011 and December 31, 2011, we obtained data from publicly available Web sites on program directors at 127 institutions that had ACGME-accredited programs in both anesthesiology and surgery. Information gathered on each individual included year of board certification, year first appointed program director, academic rank, history of NIH grant funding, and number of PubMed citations. We also calculated the h-index for a randomly selected subset of 25 institution-matched program directors. RESULTS There were no differences between the groups in number of years since board certification (P = 0.42), academic rank (P = 0.38), or years as a program director (P = 0.22). However, program directors in anesthesiology had less prior or current NIH funding (P = 0.002), fewer total and education-related PubMed citations (both P < 0.001), and a lower h-index (P = 0.001) than surgery program directors. Multivariate analysis revealed that the publication rate for anesthesiology program directors was 43% (95% confidence interval, 0.31-0.58) that of the corresponding program directors of surgical residency programs, holding other variables constant. CONCLUSIONS Program directors of anesthesiology residency programs have considerably less scholarly activity in terms of peer-reviewed publications and federal research funding than directors of surgical residency programs. As such, this study provides further evidence for a systemic weakness in the scholarly fabric of academic anesthesiology.

Once upon a time, being “in a home” was a pejorative. Now, thanks largely to the government’s uncontrolled experiment in health care reform, everyone seems to want in. At least physicians do. “Homes” are popping up everywhere. One type currently under construction and described by several articles in this month’s issue of Anesthesia & Analgesia is the “perioperative surgical home.” The perioperative surgical home concept is simple enough: better care, better service, and lower costs through standardization of the continuum of surgical care. 1 It’s a nice idea but there are at least 2 problems. One is that the ability of such health care redesign to achieve these goals is unproven. The second is that most of the cost variability in surgery comes from what happens after hospital discharge and some of the clinical conditions driving these costs are poorly understood and not readily modifiable. Cognitive outcome is a case in point. Delirium and postoperative cognitive dysfunction (POCD) are extremely common in geriatric surgical patients, 2,3 a group the government pays for because they are enrolled in Medicare. After elective major joint replacement or other types of major surgery, about 5% to 15% of elders develop delirium and 25% to 40% and 12% to 15% develop, respectively, early or late POCD. 2,4,5 This may not seem like much but it far exceeds the rate of other complications we spend a lot of time talking about and managing. Delirium and POCD are associated with prolonged length of stay, discharge to a place other than home (i.e., the physical place they actually live, not a virtual administrative home), and higher 1-year mortality (e.g., persistent delirium is associated with a 2.9-fold increase [95% confidence interval, 1.9–4.4] in mortality at 1 year). 5–8 In addition, delirium is associated with an acceler

We have previously demonstrated that aged rats have persistent impairment of spatial memory after sedation with nitrous oxide or general anesthesia with isoflurane-nitrous oxide. Propofol has different receptor mechanisms of action and a favorable short-term recovery profile, and it has been proposed that propofol is devoid of enduring effects on cognitive performance. No studies have investigated this question in aged subjects, however, so we designed an experiment to examine the long-term effects of propofol anesthesia on spatial working memory.Eighteen-mo-old rats were randomized to 2 h of 100% oxygen-propofol anesthesia (n=11) or to a control group that breathed 100% oxygen (n=10). Propofol was administered by continuous infusion via a tail vein catheter. Rats breathed spontaneously and rectal temperature was maintained. Mean arterial blood pressure was measured noninvasively and a venous blood gas was obtained just before discontinuation of propofol. After a 2-day recovery, spatial working memory was assessed for 14 days using a 12-arm radial maze. The number of total errors, number of correct choices to first error, and time to complete the maze was recorded and analyzed using a repeated measure analysis of variance (ANOVA), with P0.05 being considered statistically significant.The average propofol infusion rate was 0.6+/-0.1 mg.kg (-1).min(-1), a rate corresponding to a 50% effective concentration dose in adult rats. Mean arterial blood pressure during anesthesia was 100+/-2 mm Hg and venous blood gases remained in the normal range. There was no difference between the control and previously anesthetized rats on any measure of radial arm maze performance, indicating propofol anesthesia produces no lasting impairment in spatial working memory in aged rats.In aged rats, propofol anesthesia is devoid of the persistent memory effects observed with other general anesthetics in this model. Thus, while it appears that the state of general anesthesia is neither necessary nor sufficient for development of postanesthetic memory impairment, the choice of anesthetics may play a role in late cognitive outcome in the aged.

BACKGROUND: Nitrous oxide is a commonly used anesthetic that inhibits the activity of methionine synthase, an enzyme involved in methylation reactions and DNA synthesis and repair. This inhibition triggers vacuole formation and degeneration of neurons in areas of the developing and mature brain that are important for spatial memory, raising the possibility that nitrous oxide might have sustained effects on learning. METHODS: To test this possibility, we randomized 18-month-old Fischer 344 rats (n = 13 per group) to 4 h of 70% nitrous oxide + 30% oxygen or 70% nitrogen + 30% oxygen (control) and assessed memory using a 12-arm radial maze for 14 days beginning 2 days after nitrous oxide inhalation. In separate, identically treated groups of rats, we measured methionine synthase activity in the cortex and liver at the end of nitrous oxide exposure and 2 days later (n = 3 rats per group per time point) using a standard assay. RESULTS: Liver and cortical methionine synthase was inhibited during nitrous oxide inhalation (6% and 23% of control in liver and cortex, respectively; P < 0.01). Liver enzyme activity remained depressed 2 days later, whereas cortical enzyme activity recovered. There was no difference in error rate between control and nitrous oxide treated rats. However, those exposed to nitrous oxide took more time to complete the maze and made fewer correct choices before first error (P < 0.05). CONCLUSIONS: Sedation with 70% nitrous oxide profoundly, but transiently, reduces the activity of cortical methionine synthase but produces lasting impairment in spatial working memory in aged rats.

We have previously demonstrated that general anesthesia with 1.2% isoflurane-70% nitrous oxide impairs acquisition of a radial arm maze task in both young and aged rats when testing begins 2 days after anesthesia and in aged rats when testing begins 2 wk later. We designed this study to examine whether postanesthesia learning impairment is persistent in young rats. Six-month-old rats were randomized to anesthesia for 2 h with 1.2% isoflurane-70% nitrous oxide, 1.8% isoflurane, or a control group that received 30% oxygen (n = 10 per group). Rats recovered for 2 wk and were then tested daily on a radial arm maze for 14 days. There were no differences between the controls and anesthesia groups in number of correct choices to first error or time to complete the maze. There was no main effect of group in terms of total number of errors (P > 0.05) but the group by day interaction was significant (P < 0.05), reflecting improved performance in the 1.2% isoflurane-70% nitrous oxide group relative to controls during the later days of testing (P < 0.005). Hence, in adult rats, previous general anesthesia is not associated with impaired learning 2 wk later. In fact, previous 1.2% isoflurane-70% nitrous oxide improves maze performance 2 wk later.

From the origins of surgical anesthesia in the 1840s through the late 1990s, the prevailing view has been that the brain emerged unscathed from the assault of surgery and the pharmacologic coma we call general anesthesia. Since then, the literature has been awash in studies suggesting that is not always the case and that sometimes, in an effort to heal the body, we might be harming the brain. However, when, why, and how this happens is a matter of considerable debate. That debate is winding up rather than down and is unlikely to be resolved anytime soon. In the spirit of fueling, if not resolving, the debate, the section on Neuroscience in Anesthesiology and Perioperative Medicine in this issue of Anesthesia & Analgesia pulls together a collection consisting of original work, reviews, a meeting summary, and an opinion piece that speak to various aspects of this subject. There is something here for everyone interested in the topic, and even for those who might just be curious, but before you dive into the specific manuscripts, we thought it would be useful to put them in the context of current themes/hypotheses about adverse perioperative cognitive outcomes.