Use of a Novel Three-Dimensional Model to Teach Ultrasound-guided Subclavian Vein Cannulation.

Background: Central venous cannulation is an essential skill in perioperative and critical care medicine. Ultrasound guidance is the standard of care for femoral and internal jugular vein access, with the subclavian vein being perceived to be less amenable to ultrasound-guided (UG) insertion, resulting in a lack of procedural competency and low cannulation rate. There is a paucity of resources and a lack of experience among staff physicians to effectively instruct trainees. Simulation-based medical education has the potential to help maintain high-stakes, infrequently performed skills and counteract possible unrecognized skill decline. We aimed to create a novel, low-cost, high-fidelity three-dimensional (3D) model for UG subclavian vein (UG-SCV) access with an accompanying curriculum to improve this important skill. Methods: A curriculum was created consisting of preparatory material reviewing UG-SCV access, followed by an in-person didactic lecture focusing on ultrasound use and management of complications and a deliberate practice session scanning volunteers and practicing UG vascular puncture on a 3D model. A qualitative usability test design was used to assess the validity of the curriculum in trainees with advanced vascular access skills (anesthesiologists). Participants were second-year anesthesia residents, anesthesia fellows, and staff physicians. Focus groups conducted after each session explored the face validity of the model and curriculum. By applying a usability design, the curriculum was optimized and finalized. Results: Between September 2020 and February 2021, 28 participants tested the curriculum. The focus groups ensured that the curriculum achieved its objective, with iterative changes made after each session in a quality improvement framework Plan-Do-Study-Act approach. After the third cycle, minimal changes were suggested, and the curriculum and 3D model were finalized. An additional group of participants was used to ensure that no new input would help improve the curriculum further. Conclusions: A focused curriculum for enhancing skills in UG-SCV cannulation using a novel 3D model was successfully implemented and validated through a usability test design. This curriculum is better targeted for practitioners experienced in central venous access to master a subclavian approach and maintain their skill level.

Precontouring Plates for MIS Bilateral Femur Osteosynthesis Using a Patient-Specific 3D Printed Model: A Case Report.

CASE: A 27-year-old woman with increasing bilateral thigh pain and underlying diagnosis of dysosteosclerosis was diagnosed with bilateral impending pathological femur fractures. Both femurs exhibited abnormal morphology with bowing, thickened cortices, and narrow intramedullary canals. We planned minimally invasive prophylactic plate osteosynthesis. Computed tomography scans of both femora were obtained and used to generate 3-dimensional (3D) printed models. Osteosynthesis plates were precontoured to fit the 3D models and sterilized, and prophylactic fixation was performed using a minimally invasive submuscular technique. CONCLUSION: 3D printed models aided in precontouring fixation plates in a case with challenging bony anatomy, enabling minimally invasive surgery.

Echocardiographic assessment of left ventricular function in ex situ heart perfusion using pump-supported and passive afterload working mode: a pilot study.

Ex situ heart perfusion (ESHP) has been developed to decrease cold ischemia time and allow metabolic assessment of donor hearts prior to transplantation. Current clinical ESHP systems preserve the heart in an unloaded condition and only evaluate the cardiac metabolic profile. In this pilot study we performed echocardiographic functional assessment using two alternative systems for left ventricular (LV) loading: pump supported afterload working mode (SAM) and passive afterload working modes (PAM). Six hearts were procured from male Yorkshire pigs. During cold ischemia, hearts were mounted on our custom made ESHP circuit and a 3D-printed enclosure for the performance of echocardiography with a standard TEE probe. Following perfusion with Langherdorf mode of the unloaded heart, the system was switched into different working modes to allow LV loading and functional assessment: pump supported (SAM) and passive (PAM). Echocardiographic assessment of left ventricular function in the donor hearts was performed in vivo and at 1 h of ESHP with SAM, after 4.5 h with PAM and after 5.5 h with SAM. We obtained good quality epicardial echocardiographic images at all time points allowing a comprehensive LV systolic assessment. All indices showed a decrease in LV systolic function throughout the trial with the biggest drop after heart harvesting. We demonstrated the feasibility of echocardiographic functional assessment during ESHP and two different working modes. The expected LV systolic dysfunction consisted of a reduction in EF, FAC, FS, and strain throughout the experiment with the most significant decrease after harvesting.

The effect of diet-induced serum hypercholesterolemia on the surfactant system and the development of lung injury.

Acute respiratory distress syndrome (ARDS) is a pulmonary disorder associated with alterations to the pulmonary surfactant system. Recent studies showed that supra-physiological levels of cholesterol in surfactant contribute to impaired function. Since cholesterol is incorporated into surfactant within the alveolar type II cells which derives its cholesterol from serum, it was hypothesized that serum hypercholesterolemia would predispose the host to the development of lung injury due to alterations of cholesterol content in the surfactant system. Wistar rats were randomized to a standard lab diet or a high cholesterol diet for 17-20 days. Animals were then exposed to one of three models of lung injury: i) acid aspiration ii) ventilation induced lung injury, and iii) surfactant depletion. Following physiological monitoring, lungs were lavaged to obtain and analyze the surfactant system. The physiological results showed there was no effect of the high cholesterol diet on the severity of lung injury in any of the three models of injury. There was also no effect of the diet on surfactant cholesterol composition. Rats fed a high cholesterol diet had a significant impairment in surface tension reducing capabilities of isolated surfactant compared to those fed a standard diet exposed to the surfactant depletion injury. In addition, only rats that were exposed to ventilation induced lung injury had elevated levels of surfactant associated cholesterol compared to non-injured rats. It is concluded that serum hypercholesterolemia does not predispose rats to altered surfactant cholesterol composition or to lung injury. Elevated cholesterol within surfactant may be a marker for ventilation induced lung damage.

Cholesterol-mediated surfactant dysfunction is mitigated by surfactant protein A.

The ability of pulmonary surfactant to reduce surface tension at the alveolar surface is impaired in various lung diseases. Recent animal studies indicate that elevated levels of cholesterol within surfactant may contribute to its inhibition. It was hypothesized that elevated cholesterol levels within surfactant inhibit human surfactant biophysical function and that these effects can be reversed by surfactant protein A (SP-A). The initial experiment examined the function of surfactant from mechanically ventilated trauma patients in the presence and absence of a cholesterol sequestering agent, methyl-ß-cyclodextrin. The results demonstrated improved surface activity when cholesterol was sequestered in vitro using a captive bubble surfactometer (CBS). These results were explored further by reconstitution of surfactant with various concentrations of cholesterol with and without SP-A, and testing of the functionality of these samples in vitro with the CBS and in vivo using surfactant depleted rats. Overall, the results consistently demonstrated that surfactant function was inhibited by levels of cholesterol of 10% (w/w phospholipid) but this inhibition was mitigated by the presence of SP-A. It is concluded that cholesterol-induced surfactant inhibition can actively contribute to physiological impairment of the lungs in mechanically ventilated patients and that SP-A levels may be important to maintain surfactant function in the presence of high cholesterol within surfactant.