Virtual reality for lumbar puncture in a morbidly obese patient with leukemia.

Virtual reality is an immersive technology that can provide distraction and anxiolysis during painful procedures. While it has been shown to be effective in less invasive procedures, it is underutilized in more invasive procedures. We describe using virtual reality for a morbidly obese patient with leukemia undergoing lumbar puncture. The use of virtual reality reduced the amount of analgesics and anxiolytics and the procedure and recovery times compared with no virtual reality.

Three-Dimensional Printed Pediatric Airway Model Improves Novice Learners' Flexible Bronchoscopy Skills With Minimal Direct Teaching From Faculty.

INTRODUCTION: Training in pediatric flexible bronchoscopy (FB) is predominantly completed on patients. Early trainees are less accurate and slower than experienced bronchoscopists. This report describes the development of a three-dimensional printed airway model and describes how the model was used to teach learners basic FB skills. METHODS: Postgraduate year two (PGY2) pediatric residents completing a 1-month pediatric pulmonology rotation with minimal previous exposure to FB were randomized into a simulation trainee group (n = 18) or a control resident group (n = 9). The simulation group received four 15-minute practice sessions (3 self-directed, 1 with feedback). Participants completed a bronchoscopy assessment on the model at prestudy, poststudy, and delayed (at least 2 months after the rotation) time points. Outcomes were identification of markers located in the six lung areas and completion time. RESULTS: There was no difference in prestudy scores between groups. In the poststudy assessment, the simulation participants correctly identified more lung area markers (median = 6 vs 1.5, P < 0.001) and were faster (median = 102 vs 600 seconds, P < 0.001). In the delayed assessment, correct marker identification trended toward improvement in the simulation group compared with controls (median = 4 vs 2, P = 0.077). CONCLUSIONS: With 1 hour of practice time, requiring 15 minutes of direct teaching, novice resident bronchoscopists are able to more accurately identify and visualize the five lung lobes and lingula via FB and are able to do so in less time than control residents. This anatomically accurate model could be used to train basic FB skills at a low cost compared with other models.

Impact of residual stretch and remodeling on collagen engagement in healthy and pulmonary hypertensive calf pulmonary arteries at physiological pressures.

Understanding the mechanical behavior of proximal pulmonary arteries (PAs) is crucial to evaluating pulmonary vascular function and right ventricular afterload. Early and current efforts focus on these arteries' histological changes, in vivo pressure-diameter behavior and mechanical properties under in vitro mechanical testing. However, the in vivo stretch and stress states remain poorly characterized. To further understand the mechanical behavior of the proximal PAs under physiological conditions, this study computed the residual stretch and the in vivo circumferential stretch state in the main pulmonary arteries in both control and hypertensive calves by using in vitro and in vivo artery geometry data, and modeled the impact of residual stretch and arterial remodeling on the in vivo circumferential stretch distribution and collagen engagement in the main pulmonary artery. We found that the in vivo circumferential stretch distribution in both groups was nonuniform across the vessel wall with the largest stretch at the outer wall, suggesting that collagen at the outer wall would engage first. It was also found that the circumferential stretch was more uniform in the hypertensive group, partially due to arterial remodeling that occurred during their hypoxic treatment, and that their onset of collagen engagement occurred at a higher pressure. It is concluded that the residual stretch and arterial remodeling have strong impact on the in vivo stretch state and the collagen engagement and thus the mechanical behavior of the main pulmonary artery in calves.

Successful utilization of high-flux hemodialysis for treatment of vancomycin toxicity in a child.

Vancomycin is routinely used for empiric antibiotic therapy in children. Higher-serum-concentration targets for serious infections are now being recommended. This recommendation may result in aggressive dosing with increased potential for toxicity. We report a case of a pediatric patient who developed vancomycin toxicity and associated oliguric renal failure who was treated effectively with high-flux hemodialysis for vancomycin toxicity, clearing serum concentrations of vancomycin by over 75% in only 6 hours (213.2 mcg/mL to 51.8 mcg/mL) with subsequent return to baseline renal function and without adverse sequelae. While not historically considered a viable option for drug removal in cases of toxicity, new high-flux hemodialysis techniques can remove significant percentages of vancomycin in short periods of time.

In vivo measurement of proximal pulmonary artery elastic modulus in the neonatal calf model of pulmonary hypertension: development and ex vivo validation.

Developing clinical work suggests that vascular stiffening plays a role in the progression of pulmonary hypertension (PH), while recent studies in animal models of hypoxic PH have found significant proximal vascular stiffening in the diseased population. Here, we develop and validate a minimally invasive, clinically realizable method to estimate the local elastic modulus of the proximal pulmonary arteries from pressure-diameter (PD) data. PD measurements were made in the main pulmonary arteries of 16 calves; lumen diameter was assessed using color M-mode tissue Doppler imaging ultrasound, while pressure was measured via catheter. Two methods corresponding to thin-walled pressure vessel theory ("thin") and Lame's equation for a thick-walled cylinder ("thick") were used to approximate the artery elastic modulus from PD measurements. The harvested arteries were tested independently to determine their "true" ex vivo elastic modulus and stiffness. Both approximations displayed excellent correlation with ex vivo elastic modulus of the calf main pulmonary artery (thin r(2) = 0.811; thick r(2) = 0.844; both P < 0.01). Bland-Altman analysis indicated that the thick-walled approximation has better overall agreement with ex vivo modulus. The approximations displayed quantitatively distinct regression slopes that were statistically different (P = 0.02). The elastic modulus of the main pulmonary artery can be reasonably estimated from combined color M-mode tissue Doppler imaging ultrasound and catheter pressure measurements in calves. Such measurements may be a valuable tool in the diagnosis and treatment of human PH.

Changes in the structure-function relationship of elastin and its impact on the proximal pulmonary arterial mechanics of hypertensive calves.

Extracellular matrix remodeling has been proposed as one mechanism by which proximal pulmonary arteries stiffen during pulmonary arterial hypertension (PAH). Although some attention has been paid to the role of collagen and metallomatrix proteins in affecting vascular stiffness, much less work has been performed on changes in elastin structure-function relationships in PAH. Such work is warranted, given the importance of elastin as the structural protein primarily responsible for the passive elastic behavior of these conduit arteries. Here, we study structure-function relationships of fresh arterial tissue and purified arterial elastin from the main, left, and right pulmonary artery branches of normotensive and hypoxia-induced pulmonary hypertensive neonatal calves. PAH resulted in an average 81 and 72% increase in stiffness of fresh and digested tissue, respectively. Increase in stiffness appears most attributable to elevated elastic modulus, which increased 46 and 65%, respectively, for fresh and digested tissue. Comparison between fresh and digested tissues shows that, at 35% strain, a minimum of 48% of the arterial load is carried by elastin, and a minimum of 43% of the change in stiffness of arterial tissue is due to the change in elastin stiffness. Analysis of the stress-strain behavior revealed that PAH causes an increase in the strains associated with the physiological pressure range but had no effect on the strain of transition from elastin-dominant to collagen-dominant behavior. These results indicate that mechanobiological adaptations of the continuum and geometric properties of elastin, in response to PAH, significantly elevate the circumferential stiffness of proximal pulmonary arterial tissue.

Lung EC-SOD overexpression attenuates hypoxic induction of Egr-1 and chronic hypoxic pulmonary vascular remodeling.

Although production of reactive oxygen species (ROS) such as superoxide (O(2)(.-)) has been implicated in chronic hypoxia-induced pulmonary hypertension (PH) and pulmonary vascular remodeling, the transcription factors and gene targets through which ROS exert their effects have not been completely identified. We used mice overexpressing the extracellular antioxidant enzyme extracellular superoxide dismutase (EC-SOD TG) to test the hypothesis that O(2)(.-) generated in the extracellular compartment under hypoxic conditions contributes to PH through the induction of the transcription factor, early growth response-1 (Egr-1), and its downstream gene target, tissue factor (TF). We found that chronic hypoxia decreased lung EC-SOD activity and protein expression in wild-type mice, but that EC-SOD activity remained five to seven times higher in EC-SOD TG mice under hypoxic conditions. EC-SOD overexpression attenuated chronic hypoxic PH, and vascular remodeling, measured by right ventricular systolic pressures, proliferation of cells in the vessel wall, muscularization of small pulmonary vessels, and collagen deposition. EC-SOD overexpression also prevented the early hypoxia-dependent upregulation of the redox-sensitive transcription factor Egr-1 and the procoagulant protein TF. These data provide the first evidence that EC-SOD activity is disrupted in chronic hypoxia, and increased EC-SOD activity can attenuate chronic hypoxic PH by limiting the hypoxic upregulation of redox-sensitive genes.