Maximizing Learning in the Operating Room: Residents' Perspectives.

BACKGROUND: Few studies examine how residents can optimize their educational experience in the OR on their terms. This study aimed to examine residents' perceptions of how learners can maximize their education in the OR. METHOD: Using constructivist grounded theory methodology, the authors conducted focus groups with general surgery residents, PGY1-5, followed by semi-structured interviews with attending surgeons from a single, academic medical center. Constant comparison was used to identify themes and explore their relationships. Theoretical sampling was used until saturation was achieved. RESULTS: Residents and attendings participated. Two phases of OR learning were identified, intra-operative and inter-operative. Characters that made optimized learning included control, struggling, and reflection. Residents who practiced self-reflection with their experiences, and were able to articulate this awareness to attendings, felt the OR was an ideal learning environment. Attendings echoed similar findings. CONCLUSIONS: Providing residents with a method of maximizing OR learning is critical to postgraduate clinical education. Currently, observation passively morphs into active learning and eventually independent operating in the OR. However, residents who practice self-regulated learning, and are able to discuss their educational goals with attendings, seem to find the OR a better learning environment and progress to independence more quickly. This was echoed by practicing attendings. Providing residents with a generalizable, self-regulated learning framework specific to operative educational experiences could maximize learning potential and expedite resident progression in the OR.

Adult Intraosseous Access by Advanced EMTs: A Statewide Non-Inferiority Study.

OBJECTIVE: Intraosseous (IO) access is increasingly being used as an alternative to peripheral intravenous access, which is often difficult or impossible to establish in critically ill patients in the prehospital setting. Until recently, only Paramedics performed adult IO access. In 2014, Vermont Emergency Medical Services (EMS) expanded the Advanced Emergency Medical Technicians (AEMTs) scope of practice to include IO access in adult patients. This study compares successful IO access in adults performed by AEMTs compared to Paramedics in the prehospital setting. METHODS: All Vermont EMS patient encounters between January 1, 2013 and November 30, 2015 were examined, and 543 adult patients with a documented IO access insertion attempt were identified. The proportion of successful IO insertions was compared between AEMTs and Paramedics using a Chi-Squared statistic and a non-inferiority test. RESULTS: There was no significant difference in the percentage of successful IO access between AEMTs and Paramedics [95.2% and 95.6%, respectively; P = 0.84]. The confidence interval around this 0.4% difference (95% confidence interval = -4.2, 3.2) was within a pre-specified delta of ±10% indicating non-inferiority of AEMTs compared to Paramedics. CONCLUSIONS: This study's finding that successful IO access was not different among AEMTs and Paramedics lends evidence in support of expanding the scope of practice of AEMTs to include establishing IO access in adults.

Weight Loss Decreases Inherent and Allergic Methacholine Hyperresponsiveness in Mouse Models of Diet-Induced Obese Asthma.

Obese asthma presents with inherent hyperresponsiveness to methacholine or augmented allergen-driven allergic asthma, with an even greater magnitude of methacholine hyperresponsiveness. These physiologic parameters and accompanying obese asthma symptoms can be reduced by successful weight loss, yet the underlying mechanisms remain incompletely understood. We implemented mouse models of diet-induced obesity, dietary and surgical weight loss, and environmental allergen exposure to examine the mechanisms and mediators of inherent and allergic obese asthma. We report that the methacholine hyperresponsiveness in these models of inherent obese asthma and obese allergic asthma manifests in distinct anatomical compartments but that both are amenable to interventions that induce substantial weight loss. The inherent obese asthma phenotype, with characteristic increases in distal airspace tissue resistance and tissue elastance, is associated with elevated proinflammatory cytokines that are reduced with dietary weight loss. Surprisingly, bariatric surgery-induced weight loss further elevates these cytokines while reducing methacholine responsiveness to levels similar to those in lean mice or in formerly obese mice rendered lean through dietary intervention. In contrast, the obese allergic asthma phenotype, with characteristic increases in central airway resistance, is not associated with increased adaptive immune responses, yet diet-induced weight loss reduces methacholine hyperresponsiveness without altering immunological variables. Diet-induced weight loss is effective in models of both inherent and allergic obese asthma, and our examination of the fecal microbiome revealed that the obesogenic Firmicutes/Bacteroidetes ratio was normalized after diet-induced weight loss. Our results suggest that structural, immunological, and microbiological factors contribute to the manifold presentations of obese asthma.

Influence of distinct asthma phenotypes on lung function following weight loss in the obese.

BACKGROUND AND OBJECTIVE: There appears to be two distinct clinical phenotypes of obese patients with asthma-those with early-onset asthma and high serum IgE (TH2-high), and those with late-onset asthma and low serum IgE (TH2-low). The aim of the present study was to determine in the two phenotypes of obese asthma the effect of weight loss on small airway function. METHODS: TH2-low (n = 8) and TH2-high (n = 5) obese asthmatics underwent methacholine challenge before and 12 months following bariatric surgery. Dose-response slopes as measures of sensitivity to airway closure and narrowing were measured as maximum % fall forced vital capacity (FVC) and forced expiratory volume in 1 s/FVC, respectively, divided by dose. Resting airway mechanics were measured by forced oscillation technique. RESULTS: Weight loss reduced sensitivity to airway closure in TH 2-low but not TH2-high obese asthmatics (pre-post mean change ± 95% confidence interval: 1.8 ± 0.8 doubling doses vs -0.3 ± 1.7 doubling doses, P = 0.04). However, there was no effect of weight loss on the sensitivity to airway narrowing in either group (P = 0.8, TH2-low: 0.8 ± 1.0 doubling doses, TH2-high: -1.1 ± 2.5 doubling doses). In contrast, respiratory resistance (20 Hz) improved in TH2-high but not in TH2-low obese asthmatics (pre-post change median interquartile range: 1.5 (1.3-2.8) cmH2O/L/s vs 0.6 (-1.8-0.8) cmH2O/L/s, P = 0.03). CONCLUSIONS: TH2-low obese asthmatics appear to be characterized by increased small airway responsiveness and abnormalities in resting airway function that may persist following weight loss. However, this was not the case for TH2-high obese asthmatics, highlighting the complex interplay between IgE status and asthma pathophysiology in obesity.

Obesity and asthma: an inflammatory disease of adipose tissue not the airway.

RATIONALE: Obesity is a major risk factor for asthma; the reasons for this are poorly understood, although it is thought that inflammatory changes in adipose tissue in obesity could contribute to airway inflammation and airway reactivity in individuals who are obese. OBJECTIVES: To determine if inflammation in adipose tissue in obesity is related to late-onset asthma, and associated with increased markers of airway inflammation and reactivity. METHODS: We recruited a cohort of obese women with asthma and obese control women. We followed subjects with asthma for 12 months after bariatric surgery. We compared markers in adipose tissue and the airway from subjects with asthma and control subjects, and changes in subjects with asthma over time. MEASUREMENTS AND MAIN RESULTS: Subjects with asthma had increased macrophage infiltration of visceral adipose tissue (P < 0.01), with increased expression of leptin (P < 0.01) and decreased adiponectin (p < 0.001) when controlled for body mass index. Similar trends were observed in subcutaneous adipose tissue. Airway epithelial cells expressed receptors for leptin and adiponectin, and airway reactivity was significantly related to visceral fat leptin expression (rho = -0.8; P < 0.01). Bronchoalveolar lavage cytokines and cytokine production from alveolar macrophages were similar in subjects with asthma and control subjects at baseline, and tended to increase 12 months after surgery. CONCLUSIONS: Obesity is associated with increased markers of inflammation in serum and adipose tissue, and yet decreased airway inflammation in obese people with asthma; these patterns reverse with bariatric surgery. Leptin and other adipokines may be important mediators of airway disease in obesity through direct effects on the airway rather than by enhancing airway inflammation.

Effects of obesity and bariatric surgery on airway hyperresponsiveness, asthma control, and inflammation.

BACKGROUND: Asthma in obese subjects is poorly understood, and these patients are often refractory to standard therapy. OBJECTIVES: We sought to gain insights into the pathogenesis and treatment of asthma in obese subjects by determining how obesity and bariatric surgery affect asthma control, airway hyperresponsiveness (AHR), and markers of asthmatic inflammation. METHODS: We performed a prospective study of (1) asthmatic and nonasthmatic patients undergoing bariatric surgery compared at baseline and (2) asthmatic patients followed for 12 months after bariatric surgery. RESULTS: We studied 23 asthmatic and 21 nonasthmatic patients undergoing bariatric surgery. At baseline, asthmatic patients had lower FEV(1) and forced vital capacity and lower numbers of lymphocytes in bronchoalveolar lavage fluid. After surgery, asthmatic participants experienced significant improvements in asthma control (asthma control score, 1.55 to 0.74; P < .0001) and asthma quality of life (4.87 to 5.87, P < .0001). Airways responsiveness to methacholine improved significantly (methacholine PC(20), 3.9 to 7.28, P = .03). There was a statistically significant interaction between IgE status and change in airways responsiveness (P for interaction = .01). The proportion of lymphocytes in bronchoalveolar lavage fluid and the production of cytokines from activated peripheral blood CD4(+) T cells increased significantly. CONCLUSIONS: Bariatric surgery improves AHR in obese asthmatic patients with normal serum IgE levels. Weight loss has dichotomous effects on airway physiology and T-cell function typically involved in the pathogenesis of asthma, suggesting that obesity produces a unique phenotype of asthma that will require a distinct therapeutic approach.

Travel distance as factor in follow-up visit compliance in postlaparoscopic adjustable gastric banding population.

BACKGROUND: Despite the 2008 "American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic and Bariatric Surgery Medical Guidelines for Clinical Practice for the Perioperative Nutritional, Metabolic, and Nonsurgical Support of the Bariatric Surgery Patient," consensus does not exist for postoperative care in laparoscopic adjustable gastric banding (LAGB) patients (grade D evidence). It has been suggested that regular follow-up is related to better outcomes, specifically greater weight loss. The aim of the present study was to investigate the effects of travel distance to the clinic on the adherence to follow-up visits and weight loss in a cohort of LAGB patients in the setting of a rural, university-affiliated teaching hospital in the United States. METHODS: A retrospective chart review was performed of all consecutive LAGB patients for a 1-year period. Linear regression analysis was used to identify the relationships between appointment compliance and the distance traveled and between the amount of weight loss and the distance traveled. RESULTS: Linear regression analysis was performed to investigate the effect of the travel distance to the clinic on the percentage of follow-up visits postoperatively. This effect was not significant (P = .4). Linear regression analysis was also performed to elucidate the effect of the travel distance to the clinic on the amount of weight loss. This effect was significant (P = .04). CONCLUSION: The travel distance to the clinic did not seem to be a significant predictor of compliance in a cohort of LAGB patients with ≤ 1 year of follow-up in a rural setting. However, a weak relationship was found between the travel distance to the clinic and weight loss, with patients who traveled further seeming to lose slightly more weight.

Pressure-induced cellular senescence: a mechanism linking venous hypertension to venous ulcers.

INTRODUCTION: Slow healing of ulcers in chronic venous insufficiency (CVI) has long been thought secondary to venous hypertension. Dermal fibroblasts isolated from venous ulcers have morphologies and protein production suggestive of premature aging. In this study, we hypothesized that neonatal fibroblasts (NNF) cultured under elevated pressure will demonstrate premature aging and that this effect will be augmented by an inflammatory mediator, transforming growth factor beta (TGF-beta). MATERIALS AND METHODS: A unique pressure incubator was used to culture NNF at atmospheric pressure (ATM), ATM + 30 mmHg, ATM + 60 mmHg, and ATM +120 mmHg. Some pressure-exposed NNF were also cultured with TGF- beta (1 ng/ml). Growth rates were determined by flow cytometry. Senescent cells were identified by staining with a marker for cellular senescence, beta-galactosidase (SA-beta-Gal). Light microscopy and digital imaging were used to evaluate cell morphology. Paired linear models and comparison of the slopes were used for statistical analysis of growth. chi2 analysis was used to compare senescence rates. RESULTS: NNF cultured at ATM + 60 mmHg and ATM + 120 mmHg showed increased SA-beta-Gal activity (P <0.05), and reduced growth rates (P <0.05) at 11 days. These effects were not seen at ATM + 30 mmHg. NNF grown with TGF-beta did not show augmented SA-beta-Gal staining. CONCLUSIONS: Pressure-exposed NNF demonstrated an accelerated aging phenomenon similar to fibroblasts isolated from venous ulcers. This aging effect was directly related to the level of pressure. TGF-beta did not augment the aging effect. This study suggests that pressure elevations result in altered cell function and accelerated aging that may contribute to the slowed healing seen in patients with venous insufficiency.

A new in vitro model of venous hypertension: the effect of pressure on dermal fibroblasts.

PURPOSE: Venous hypertension leads to venous stasis ulcers. White cell activation, protein leakage from pressurized capillaries, and cytokine imbalances have all been implicated as indirect effects of venous hypertension that contribute to dermal changes seen in chronic venous insufficiency. The direct effect of increased tissue pressures on dermal elements has not been investigated. Prior studies have shown that fibroblasts isolated from venous ulcers have altered growth rates, morphologies, and protein production similar to senescent or aged fibroblasts. We hypothesize that neonatal fibroblasts (NNFs) cultured in conditions of increased atmospheric pressure will demonstrate altered cell function when compared with those grown at normal atmospheric pressure (ATM). METHODS: A pressure incubator was used to culture populations of NNFs at ATM, 60 mm Hg over ATM (ATM + 60 mm Hg), and 120 mm Hg over ATM (ATM + 120 mm Hg). NNF population growth rates were determined by periodic flow cytometry analysis over a 2-week period. Light microscopy and digital imaging were used to evaluate cell morphology. Senescence-associated B-galactosidase (SA-beta-Gal) activity was determined using the X-Gal stain. Fibronectin production was assessed by exposing cells sequentially to anti-fibronectin antibodies and Oregon Green-conjugated goat anti-mouse secondary antibodies. Flow cytometry then was used to determine relative proportions of cells staining positively for fibronectin. Statistical analysis was accomplished with analysis of variance. RESULTS: Populations of cells grown under increased pressures (both ATM + 60 and ATM + 120) showed reduced growth rates (P <.001). Similarly, morphologies of cells grown under pressure had increased cytoplasm to nuclear ratios with abnormal nuclear shapes. Populations of cells grown under pressure had higher percentages of cells staining positive for fibronectin (ATM = 45%, ATM + 60 = 59%, ATM + 120 = 79%). After 14 days of growth under pressure, fibroblast populations did not demonstrate augmented productions of the senescence marker SA-beta-Gal (ATM =.5%, ATM + 60 =.25%, ATM + 120 =.75%). CONCLUSIONS: This study demonstrated that NNFs grown in culture under increased pressures undergo a transformation not seen in cells grown at atmospheric pressure. Cells grown under pressure demonstrated reduced growth rates, increased fibronectin production, and abnormal morphologies similar to fibroblasts isolated from venous ulcers. This study suggests that pressure elevations (like venous hypertension) can directly result in altered cell function and morphology that may contribute to the delayed wound healing seen in patients with venous ulcers. This model uses a pressurized incubator that may prove to be a valuable adjunct in studying the effects of venous hypertension.