( Can J Anesth/J Can Anesth. (2023) 70:811–816) This editorial refers to a recent case published by Dr Pysyk and Dr Filteau describing an inadvertent administration of tranexamic acid into the epidural space. The authors of the editorial discuss this case involving a medication error and propose mechanisms to prevent similar errors in the future. While the error was recognized and managed without immediate adverse effects, the potential for catastrophic consequences was highlighted.

He is survived by his wife, Sallie, herself an accomplished cardiac anesthesiologist, three children, and seven grandchildren

Medical regulatory colleges have a mandate to protect and promote the health and safety of the public by regulating the practice of medicine by physicians. In Canada, provincial colleges of physicians and surgeons fulfill this mandate through activities related to a) the registration of physicians to practice, b) the regulation of how physicians practice (either proactive or reactive regulatory activities), and c) remediation of physicians where specific deficiencies are identified and where remediation is appropriate. Throughout most of the 150-year history of selfregulation of the medical profession in Canada, this role has been performed primarily by reactive regulation, i.e., disciplining physicians who have been found to be practicing in a manner that members of the profession would consider to be dishonourable, disgraceful, or unprofessional. As important as remediation may be, the disciplinary process remains a key means of maintaining the public trust in the profession. This is reactive regulation, as it results from a specific complaint, inquiry, or report to the college about a physician’s behaviour or performance. It is important to emphasize that most colleges have remediation programs that manage clinical practice deficiencies identified during the complaint process. Disciplinary procedures are invoked only when major unprofessional practices are found. By law, the college’s disciplinary proceedings and outcomes are transparent to the public. Disciplinary findings result from a formal adversarial legal process after an extensive investigation of the merits of the allegations. Formal charges are filed, and the physician involved is allowed to mount a thorough defense to the allegations. Although individual disciplinary findings are published by each provincial regulatory body, the report presented by Alam et al. in this issue of the Journal is the first systematic evaluation of disciplinary findings against anesthesiologists in Canada. The report follows the publication of their data on all disciplined physicians in Canada from 2000-2009. The authors conclude that publication of the causes of disciplinary actions may result in ‘‘interventions aimed at educating physicians around standard of care’’ and prevent such problems. Whether education can prevent such serious lapses of professionalism remains speculative at best, but their data give us the first specialty-specific, national perspective on this important issue. Their first contribution is to compare the scope of the problem for anesthesiologists with that for all physicians in Canada. They emphasize that there were 721 disciplinary findings against physicians of all specialties in Canada from 2000-2011, whereas only 11 findings were against anesthesiologists. This frequency represents disproportionately fewer anesthesiologists than many other specialties. This result differs from the report from California’s State Medical Board where anesthesiologists were overrepresented among disciplined physicians. Complaints that reach the Discipline Committee represent only 2-3% of the total number of patient complaints about physicians. This number probably The author is a member of Council of the College of Physicians and Surgeons of Ontario and has no other competing interests to declare.

Planning human resources in any healthcare sector and in anesthesiology, in particular, is a complex task. Human resource planning (HRP) indicators, such as the physician to population ratio, physician utilization, and job vacancy rates, reflect supply and do not consider patients’ needs for physician services. A major component of planning for an adequate future supply of practitioners, in any jurisdiction, is an understanding of factors that contribute to the retention or loss of trainees within the specific province or territory being considered. In this issue of the Journal, Suess et al. provide some unique insights into our understanding of this aspect of supply. They examine the origin and destination of anesthesiology residents who trained in the same city, in two separate university programs, and in two different languages, and who graduated between 1990 and 2010. The past two decades in Canada were seen as a period of widespread shortage of anesthesiologists during which a number of system changes occurred. These system changes affected patients (with growing wait times for surgery) and involved governments (increased expenditures on physician reimbursement and mandated labour mobility acts), hospitals (increased use of the Anesthesia Care Team model), teaching institutions (distributed medical education and new remote university departments and programs), educational and regulatory colleges (increased eligibility of international graduates to Royal College examinations and National Standards for accreditation), and certainly anesthesiologists who devote the best part of their lives to the profession. In Ryten’s report on anesthesia human resources published in 2000—which became the basis of a thorough workforce planning model— it was emphasized that, ‘‘in order to understand the many dynamic factors in play, it is important to examine the flow of anesthesiologists – the ongoing additions and losses to the stock – and equally important, the reasons for the flows’’. In this issue of the Journal, Suess et al. contribute to our current understanding of the determinants of the ‘‘stock of providers’’ trained in Canada. Despite lack of consensus among these components of the system, residency programs within medical schools must decide who should be offered positions in anesthesia and how these physicians should be educated. In making these decisions, universities must respond to the needs of the society they serve, and they must also maintain their internal consistency as institutions devoted to maintaining and generating a body of knowledge in their specific program areas. To simplify the picture, universities can be seen as serving two masters: the students, who seek to complete their education in a specific area; and society, which depends on the skills acquired by the students. When the goals and objectives of both parties merge, no problem exists; programs may choose the brightest most dedicated candidates who will provide the highest quality services to society once their training is finished. In anesthesiology, a fine balance between supply and demand seems achievable. There is no shortage of motivated medical students who F. Donati, MD, PhD (&) Departement d’anesthesiologie, Universite de Montreal, Montreal, QC, Canada e-mail: francois.donati@umontreal.ca

Objectives: Intravasation of bone marrow contents into venous circulation and pulmonary embolization after intramedullary nailing may be coupled with the activation of coagulation and fibrinolytic cascades. The objective of this study was to assess hemostatic response to pulmonary extravasated marrow contents. We hypothesize that activation of platelet activity and the coagulation cascade may occur after embolization of marrow contents in an experimental animal model of intramedullary nailing.Methods: Fifteen New Zealand white male rabbits were randomly assigned to control or fat embolism (FE) groups. In the FE group (n = 8), femurs were surgically instrumented with retrograde intramedullary nails and pressurized with bone cement. In the control group (n = 7), a sham knee incision was made that was immediately closed without drilling, reaming, or pressurization. Fibrinogen, D-dimer latex screen assay, 1 stage prothrombin time, and activated partial thromboplastin time were analyzed.Results: As the main platelet activation indicators, the marker Annexin-V percent binding increased in the FE group at 2 hours (P = 0.04) and 4 hours (P = 0.04), and the marker CD62P percent expression increased in the FE group at 2 hours (P = 0.04).Conclusions: This preliminary study showed that pressurization of marrow and intravasation of fat and marrow products cause activation of platelets and the coagulation cascade, with or without tissue trauma. This may be relevant to the treatment of multiply injured patients with prior respiratory and coagulation abnormalities. A future larger study may be needed.

Objectives: The objective of this study was to assess the effects of fat embolism on rabbit physiology.Methods: After anesthetic administration, both femoral condyles of the right knee only of 23 New Zealand white rabbits were exposed through a medial parapatellar approach to the knee. In the pulmonary fat embolism group (n = 15), the femoral canal was drilled in a retrograde fashion and then reamed and pressurized with a 1- to 1.5-mL cement injection. In the no-pressurization group (n = 4), after reaming, no cement was injected. In the control group (n = 4), the knee incision was immediately closed. Animals were then observed for 5 hours. Hemodynamics and blood gases were recorded at standard intervals. Postmortem, the lungs were removed en bloc and fixed for histologic assessment and quantitative histomorphometry.Results: Four intraoperative deaths occurred in the pulmonary fat embolism group immediately after pressurization and may have been associated with hypotension and cardiac arrest. In the pulmonary fat embolism group, pulmonary artery pressure increased, and both mean arterial pressure and PaO2 decreased after pressurization. Approximately 2% of lung volume was occupied by intravascular fat and there were no signs of perivascular inflammation. Control and no-pressurization animals remained stable throughout the experiment.Conclusions: This model simulates pulmonary fat embolism after long-bone fractures. Despite cardiorespiratory dysfunction, there was no evidence of fat initiating pulmonary inflammation based on histologic data within the timeframe of the investigation.

BACKGROUND:The objective of this study was to assess the role of pulmonary fat embolism caused by intramedullary pressurization of the femoral canal in the development of acute lung injury in the setting of acute hemorrhagic shock and resuscitation.METHODS:Thirty New Zealand White rabbits were randomly assigned to one of four groups: (1) nine animals in which hemorrhagic shock was induced by carotid bleeding, resuscitation was performed, and the femoral canal was reamed and pressurized with bone cement to induce fat embolism (hemorrhagic shock and resuscitation/fat embolism [HR/FE] group); (2) six animals in which shock was induced by carotid bleeding, resuscitation was performed, and a sham knee incision was made and closed without drilling, reaming, or pressurization (hemorrhagic shock and resuscitation [HR] group); (3) eight animals in which no hemorrhage or shock was induced but the femoral canal was reamed and pressurized with bone cement to induce fat embolism (fat embolism [FE] group); and (4) seven animals that had a three-hour ventilation period followed by a sham knee incision (control group). The animals were ventilated for four hours following closure. Flow cytometry with use of antibodies against CD45 and CD11b was performed to test neutrophil activation in whole blood. Histological examination of lung specimens was also performed. Plasma and bronchoalveolar lavage fluid were analyzed for monocyte chemotactic peptide-1 and interleukin-8 levels with use of the ELISA (enzyme-linked immunosorbent assay) method.RESULTS:Three animals in the HR/FE group died immediately after canal pressurization and were excluded. CD11b mean channel fluorescence was significantly elevated, as compared with baseline, only in the HR/FE group at two hours (p = 0.025) and four hours (p = 0.024) after knee closure. Histological analysis showed that only the HR/FE (p < 0.001) and HR (p = 0.010) groups had significantly greater infiltration of alveoli by polymorphonuclear leukocytes as compared with that in the controls. No significant differences in plasma cytokine levels were found between the groups. Only the HR/FE group had significantly higher interleukin-8 (p = 0.020) and monocyte chemotactic peptide-1 (p = 0.004) levels in the bronchoalveolar lavage fluid as compared with those in the controls.CONCLUSIONS:Fat embolism from canal pressurization alone did not activate a pulmonary inflammatory response. The combination of hemorrhagic shock, resuscitation, and fat embolism elicited neutrophil activation, infiltration of alveoli by polymorphonuclear leukocytes, and inflammatory cytokine expression in bronchoalveolar lavage fluid.

Background: The objective was to investigate changes in pulmonary blood flow after lung contusion and fat embolism. Methods: Eighteen mongrel dogs were randomly assigned to three groups: fat embolism alone (n = 7); moderate unilateral pulmonary contusion followed by fat embolism (n = 6); and severe unilateral pulmonary contusion followed by fat embolism (n = 5). Fat embolism was produced by intramedullary reaming of left femur and tibia followed by canal pressurization using bone cement. Outcome measures were systemic blood pressure, pulmonary artery pressure, pulmonary artery occluded pressure, cardiac output (CO), and partial pressures of arterial and mixed venous oxygen (Pao2, PvO2). Samples were taken from contused and noncontused contralateral lung to calculate regional pulmonary blood flow. Results: After the fat embolism, pulmonary artery pressure and pulmonary vascular resistance increased significantly (p < 0.05) in all groups, whereas Pao2 decreased in groups 2 and 3 and at 30 minutes in group 1. CO decreased significantly in group 3. Group 3 also demonstrated a greater initial decrease in Pao2 and PvO2 from baseline and a larger increase in pulmonary vascular resistance. In those animals that underwent contusion, regional pulmonary blood flow was not found to be different between contused and noncontused lung segments. After contusion, flow decreased significantly in contused and noncontused segments in group 3 only. Conclusions: Gas exchange deteriorates because of decreased CO. For any preexisting intrapulmonary shunt, the decrease of PvO2 will cause worsening of Pao2.

It is remarkable that 40 years have elapsed since Denson and Abrahamson first introduced high fidelity simulation (Sim One) to facilitate the teaching of endotracheal intubation and the induction of anesthesia. The concept of utilizing a simulator for clinical training was far ahead of its time and not immediately embraced by anesthesiologists or other educators. Simulation technology for medical education underwent a revival in the mid-1980s when computer-generated screen based simulation programs made their appearance, focusing primarily on pharmacology and physiology applications relevant to anesthesia. The anesthesiologist could choose one of many scenarios that might be encountered by a clinical anesthesiologist. These programs allowed the learner to interpret information and make pharmacological and therapeutic decisions. Such simulators were novel and afforded a meaningful learning experience, especially for novice learners; however, they did not duplicate the application of practical skills and knowledge in a clinical environment in real time. In 1986, Gaba et al. at Stanford University developed a full-scale, high fidelity simulator (‘‘The Comprehensive Anesthesia Simulation Environment [CASE]’’) which allowed the anesthesiologist to manage critical situations. With Jeff Cooper in Boston, they developed an organized program called ‘‘Anesthesia Crisis Resource Management’’ (ACRM), applying principles from the airline industry where pilots and airline crew use ‘‘Crew Resource Management’’ programs to elicit human responses in a realistic environment. The objective of ACRM is to teach participants the importance of non-technical skills such as team working, task management, decision-making and situation awareness, focusing on communication and leadership skills. In the late 90s, several simulation centres appeared in Canada, led by anesthesiologists, to allow learners to practice difficult and rare scenarios without placing patients at risk. Today, simulation centres have been developed in over 50 centres across Canada, including many community colleges, in addition to hospitals and universities. In spite of the exponential growth of simulation, many professions and disciplines have been slow to recognize that simulationbased education is more than a teaching tool—it is a novel form of ‘‘experiential education’’, with which non-technical skills required in professional practice can be learned. Educators know that these are difficult (if not impossible) to teach in the clinical environment. Most Canadian academic departments of anesthesia have been progressive in integrating simulation into the undergraduate and/or postgraduate curricula. Undergraduate medical students who are given time in an anesthesia simulator, enthusiastically compete with each other to manage the airway, and pharmacologically treat simple hemodynamic problems. It is often their first opportunity to independently treat a ‘‘patient problem’’ and the majority find it very enjoyable and a great learning experience. At the postgraduate level, simulators are used to teach firstyear residents how to ‘‘troubleshoot’’ the anesthesia gas machine through clinically relevant scenarios, and manage common intraoperative anesthetic problems. Postgraduate years 2–5 often spend at least two, three-hour sessions each year in the simulation center. They usually share this experience in a small group and are usually not in the same R. J. Byrick, MD (&) V. N. Naik, MD Department of Anesthesia, St. Michael’s Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada e-mail: robert.byrick@utoronto.ca

Résumé Objectif Décrire un cas d’embolie graisseuse survenu suite à une chirurgie élective de relâchement de contracture du tendon chez un patient souffrant de dystrophie myotonique, et souligner l’importance de la prise en compte de ce syndrome dans le diagnostic différentiel de dysfonctionnement neuro-cognitif postopératoire aigu. Éléments cliniques Un homme de 34 ans souffrant de dystrophie myotonique a été opéré sans incident sous anesthésie régionale pour relâcher la contracture d’un tendon. Immédiatement après l’opération, des complications neurologiques et respiratoires sont apparues, nécessitant une admission aux soins intensifs. Le patient a manifesté la triade clinique classique associée à l’embolie graisseuse : hypoxémie, déficit neurologique et pétéchies. Un diagnostic d’embolie graisseuse a été établi mais, malgré un traitement à base de liquides intraveineux et d’inotropes, le patient est décédé. Il n’y avait pas de shunt intracardiaque établi, ce qui aurait suggéré qu’un shunt intrapulmonaire physiologique aurait pu être responsable du développement de manifestations systémiques d’embolie graisseuse. Conclusions Le dysfonctionnement neurologique postopératoire est un état difficile ayant de nombreuses causes possibles. Toutes les étiologies possibles, y compris l’embolie graisseuse, doivent être prises en compte dans le diagnostic différentiel et dans la prise en charge postopératoire des patients qui développent un déficit neurologique aigu postopératoire et de l’hypoxémie.

PURPOSE:To describe a case of fat embolism syndrome (FES) following elective tendon contracture release in a patient with myotonic dystrophy, to highlight the importance of considering this entity in the differential diagnosis of acute postoperative neurocognitive dysfunction.CLINICAL FEATURES:A 34-yr-old man with myotonic dystrophy underwent uneventful tendon contracture release under regional anesthesia. In the immediate postoperative period, neurological and respiratory complications developed, requiring intensive care support. The patient showed the classical clinical triad of hypoxemia, neurological impairment and a petechial rash associated with the FES. A diagnosis of FES was made and, despite therapy including fluid and inotropic support, the patient succumbed to the condition. There was no demonstrated intracardiac shunt, suggesting a physiological intrapulmonary shunt was responsible for the development of systemic manifestations of FES.CONCLUSIONS:Postoperative neurological dysfunction is a difficult condition with numerous possible causes. All possible etiologies, including FES, need to be considered in the differential diagnosis and postoperative management of patients developing acute postoperative neurological impairment and hypoxemia.