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This article discusses modernizing the education of pediatric anesthesiologists in the United States. First, the current education requirements to become an American Board of Anesthesiology certified pediatric anesthesiologist are detailed and then, through a historical lens, the development of the subspecialty is examined. Gaps and challenges in the current training system are identified and interventions for improvement discussed. Additionally, suggestions are made and questions posed on how to move from a time-based model towards a competency-based curriculum.

Additional file 1. Sim tech skills fellow exam.

Intraoperative accidental extubation on a known difficult-airway patient requires prompt attention. A good understanding of the steps to re-establish the airway is critical, especially when the patient is known to have a difficult airway documented or discovered on induction or acquires a difficult airway secondary to intraoperative events. The situation becomes even more complicated if the case has been handed off to another anesthesiologist, where specific and detailed information may not have been conveyed. This simulation was designed to train first-year clinical anesthesia residents. It was a 50 min encounter that focused on the management of complete loss of an airway during a thyroidectomy on a known difficult-airway patient. The endotracheal tube dislodgement was simulated by deliberate tube manipulation through the cervical access window of the mannequin. Learners received a formative assessment of their performance during the debrief, and most of the residents met the educational objectives. Learners were asked to complete a survey of their experience, and the feedback was positive and constructive. The response rate was 68% (17/25). Our simulation program helped anesthesiology residents develop intraoperative emergency airway management skills in a safe environment, as well as foster communication skills among anesthesiologists and the surgery team.

Anesthesiologists may encounter multiple obstacles in communication when attempting to collect information for emergency surgeries. Occult tension pneumothorax that was asymptomatic in the emergency department (ED) could become apparent upon positive pressure ventilation and pose a critical threat to the patient intraoperatively. Here, we describe a simulation exercise that was developed as a curriculum module for the Indiana University (IU) Anesthesiology residency program. It is primarily designed for first-year clinical anesthesia residents (CA-1/PGY-2). It is a 50 min encounter with two scenarios. The first scenario focuses on information collection and communication with a non-cooperative patient with multiple distractors. The second scenario focuses on the early diagnosis of tension pneumothorax and subsequent treatment. The residents were given formative feedback and met the educational objectives. Commonly missed critical actions included misdiagnosing the tension pneumothorax as mainstem intubation, bronchospasm, pulmonary thromboembolism, and anaphylaxis. Residents rated the feedback and debriefing as “extremely useful” or “very useful.” Time constraints limit the number of residents who can sit in the “hot seat.” The structure of the mannequin limits the ability to diagnose pneumothorax by auscultation and ultrasound. In the future, the scenarios may also be utilized to educate student anesthesiologist assistants and other non-physician anesthesia learners.

BACKGROUND Concern about the effects of inhaled, halogenated anesthetics on neurodevelopment of infants has renewed interest in regional anesthesia as an alternative to general anesthesia (GA). Infants undergoing percutaneous Achilles tenotomy (PAT) are well suited for spinal anesthesia (SP). METHODS Thirty infants (mean age: 2.3 mo) undergoing PAT with SP were compared with 15 infants (mean age: 2.0 mo) undergoing PAT with GA. Data collected included perioperative times, heart rate and blood pressure, and the administration of opioids. RESULTS Ten of 15 GA (67%) patients received perioperative opioids as opposed to 1 of 30 SP patients (3.3%) (P

Introduction Sepsis is a major cause of morbidity and mortality in medicine and is managed in ICUs daily. Critical care training is a vital part of anesthesiology residency, and understanding the presentation, management, and treatment of septic shock is fundamental to intraoperative patient care. Methods This simulation involved a 58-year-old man undergoing surgical debridement of a peripancreatic cyst with hemodynamic instability and septic shock. We conducted the simulation yearly for clinical anesthesia year 2 residents (n = 26) in 1-hour sessions with three to five learners at a time. The simulation covered the six Anesthesiology Milestones related to sepsis and septic shock as outlined in the Anesthesiology Milestones Project. Results To date, 155 anesthesiology residents have completed the simulation. Commonly missed critical actions included failure to recognize the need for invasive lines, provide appropriate volumes of fluid resuscitation, inquire about blood cultures and antibiotics, and recognize the need for the patient to remain intubated. Most participants could appropriately diagnose and treat intraoperative septic shock, but all had moments of action or inaction to discuss and improve upon, and all learned from this scenario. Discussion Simulation is an optimal way to practice the more rare and life-threatening clinical events in medicine. Even though septic shock is commonly managed in the ICU, it is relatively uncommon for it to develop acutely in the OR. This simulation is an effective and educational way to discuss the most recent sepsis/septic shock definition and review evidence-based guidelines for treatment.

The coronavirus disease 2019 (COVID-19) pandemic has rapidly exposed health care system inadequacies. Hospital ventilator shortages in Italy compelled US physicians to consider creative solutions, such as using Y-pieces or T-pieces, to preclude the need to make decisions of life or death based on medical equipment availability. We add to current knowledge and testing capacity for ventilator splitters by reporting the ability to examine the functionality of ventilator splitters by using 2 high-fidelity lung simulators. Data obtained by the high-fidelity lung simulators included: tidal volume, respiratory rate, minute ventilation, peak inspiratory pressure, peak plateau pressure, and positive end-expiratory pressure.

Background Patients with allergic asthma have symptoms of a predominant T H 2 response, including airway eosinophilic inflammation and increased mucous production in the lungs. This accompanies increased airways responsiveness, which can be life threatening. Because T H 2 cells and cytokines have been implicated in contributing to these symptoms, pathways that control the development of these cells or that regulate their cytokine production represent good targets for controlling this disease. Objective We have previously shown that mice lacking the tyrosine kinase inducible T-cell kinase (ITK) have drastically reduced airway inflammation in a model of allergic asthma. However, it was not clear whether this translated into reduced airways hyperresponsiveness. We have analyzed tracheal responsiveness and airways hyperresponsiveness of wild-type (WT) and ITK null mice during induction of experimental allergic asthma. Methods Experimental allergic asthma was induced in WT and ITK knockout mice. Tracheal responses to carbachol, acetylcholine, and potassium chloride were analyzed. Airways hyperresponsiveness to methacholine challenge was also analyzed in allergen-challenged mice, along with lung and bronchoalveolar lavage fluid T H 2 cytokine message and protein. Results ITK null mice have reduced tracheal responses to cholinergic challenge in vitro before as well as after allergen challenge. These mice also have reduced airways hyperresponsiveness in response to allergen challenge, which could be rescued by transferring WT splenocytes or purified WT CD4 + T cells. This reduced airways response was preferentially accompanied by reduced expression of T H 2 cytokines in the lungs. Conclusion Our results indicate that the tyrosine kinase ITK and its function in T cells represent an attractive target for antiasthmatic drugs. Clinical implications Modulating the expression or activity of ITK may be a novel strategy to block allergic airway inflammation.

It has been shown that the Tec family nonreceptor tyrosine kinase inducible T cell kinase (ITK) plays a role in the activation of naive T cells and in the differentiation of T helper (T H 2)-type cells producing cytokines in a model of allergic inflammation, thereby possibly indirectly mediating hyperresponsivenes of airway smooth muscle tone. Using excised tracheae from wild type (WT) mice and those lacking ITK, we conducted a series of in vitro experiments in which isometric smooth muscle tones were assessed in response to several agonists to determine whether the absence of ITK would affect the responsiveness of tracheal smooth muscle cells. The resulting change in contractile responses was evaluated by measuring agonist cumulative concentration-response curves (CCRC). Our results indicate that the cholinergic agonist acetylcholine (ACh) and its analog carbachol (CCh) exhibited comparable CCRC profiles in contracting isolated tracheae from both WT and ITK −/− mice, with no alteration in their efficacies. However, the EC 50 values for the two agonists were found to be significantly higher in ITK −/− tracheae than in those from WT mice, suggesting an alteration of the potencies of these cholinergic agonists in the trachea of ITK −/− mice. Moreover, we found that the depolarizing agent potassium chloride (KCl) had a significantly lower efficacy in contracting ITK −/− tracheae compared to those from WT mice. This difference in KCl efficacy was abolished in the presence of a calcium (Ca 2+ ) voltage-dependent channel (VDC) agonist, Bay K8644, suggesting a modulation of the KCl induced permeability of VDC Ca 2+ channels in the trachea of ITK −/− mice. Taken together, these results suggest that the presence of ITK may play a modulating role in the pharmacomechanical as well as in the electromechanical coupling of airway smooth muscle contraction.

A retrospective study of 379 consecutive patients who underwent operative repair of facial fractures at the West Virginia University Medical Center was carried out. Blindness developed in at least one eye in 21 (6%) of the 379 patients studied. Le Fort II and Le Fort III fractures, frontal bone and frontal sinus fractures, severe fractures of the zygoma, and fractures of the orbital floor were associated with fractures of the lesser sphenoid wing and optic canal in 5 of the patients studied. These 5 patients had indirect optic nerve injuries, as determined by CT scan and clinical criteria, which included visual loss with afferent pupillary defect and an otherwise normal ophthalmologic examination. In addition, one other patient who was not one of the 379 patients who underwent operative repair gradually developed ipsilateral blindness as a result of indirect optic nerve injury following minimal frontal bone trauma without a fracture. The usual mechanism of injury was trauma at the level of the orbital roof. The principal findings on CT scan were those of fracture of the lesser sphenoid wing and subdural hematoma of the optic nerve sheath. The association between sphenoethmoid sinus hemorrhage and fracture of the optic canal (31%) in cases of facial trauma has been presented. The indications for optic nerve decompression have been discussed. To the authors' knowledge, there is no previous report of an optic canal fracture as diagnosed by computerized tomography in the literature.