Current use of the National Surgical Quality Improvement Program surgical risk calculator in academic surgery: a mixed-methods study.

Background: This study aims to quantitatively assess use of the NSQIP surgical risk calculator (NSRC) in contemporary surgical practice and to identify barriers to use and potential interventions that might increase use. Materials and methods: We performed a cross-sectional study of surgeons at seven institutions. The primary outcomes were self-reported application of the calculator in general clinical practice and specific clinical scenarios as well as reported barriers to use. Results: In our sample of 99 surgeons (49.7% response rate), 73.7% reported use of the NSRC in the past month. Approximately half (51.9%) of respondents reported infrequent NSRC use (<20% of preoperative discussions), while 14.3% used it in ≥40% of preoperative assessments. Reported use was higher in nonelective cases (30.2% vs 11.1%) and in patients who were ≥65 years old (37.1% vs 13.0%), functionally dependent (41.2% vs 6.6%), or with surrogate consent (39.9% vs 20.4%). NSRC use was not associated with training status or years in practice. Respondents identified a lack of influence on the decision to pursue surgery as well as concerns regarding the calculator's accuracy as barriers to use. Surgeons suggested improving integration to workflow and better education as strategies to increase NSRC use. Conclusions: Many surgeons reported use of the NSRC, but few used it frequently. Surgeons reported more frequent use in nonelective cases and frail patients, suggesting the calculator is of greater utility for high-risk patients. Surgeons raised concerns about perceived accuracy and suggested additional education as well as integration of the calculator into the electronic health record.

Higher Inpatient Mortality for Women after Intervention for Lifestyle Limiting Claudication.

BACKGROUND: Sex-related differences in outcomes have been identified in patients with peripheral artery disease (PAD). We hypothesized that women with PAD would have equivalent inpatient mortality with men after vascular intervention. METHODS: Patients with a primary diagnosis of critical limb ischemia (CLI) or lifestyle-limiting claudication (LLC) receiving endovascular (EV) or open surgical repair from 2003-2012 were identified from the Nationwide Inpatient Sample. Demographics, comorbidities, and inpatient mortality were analyzed by chi-squared tests of independence and independent-samples t-tests. Logistic regression analysis was performed to identify predictors of inpatient mortality. SPSS 24 software was used with P < 0.05 considered statistically significant. RESULTS: We identified 139,435 (59,432 women and 80,003 men) individuals meeting the aforementioned criteria. Women were older than men (71.5 years vs. 68.2, P < 0.001). There were no differences in racial distribution but women had lower rates of diabetes (38.6% vs. 39.7%, P < 0.001), chronic obstructive pulmonary disease (17.9% vs. 19.5%, P < 0.001), and coronary artery disease (38.6% vs. 47.4%, P < 0.001), while having a higher rate of hypertension (60.0% vs. 56.1%, P < 0.001). There was no sex-related difference in the rate of chronic renal failure. Women had higher inpatient mortality than men after vascular intervention (1.3% vs. 1.1%, P < 0.001). When stratified by surgical technique, women also had higher inpatient mortality after EV repair (1.0% vs. 0.8%, P < 0.05) and open repair (1.9% vs 1.3%, P < 0.001). When separated by admitting diagnosis, women with CLI had higher inpatient mortality than men after open surgery (2.3% vs. 1.9%, P < 0.05) but not after EV intervention. Women with LLC had higher inpatient mortality after both open (0.6% vs. 0.3%, P < 0.05) and EV surgery (0.3% vs. 0.1%, P < 0.05). Regression analysis revealed female sex as an independent predictor of inpatient mortality in patients with LLC (OR, 1.74; 95% CI 1.30-2.32, P < 0.001) but not CLI. CONCLUSIONS: Women had higher inpatient mortality than men after vascular intervention for PAD. Women were also older and more likely to have EV intervention than men. Subgroup analysis suggests that these sex-related differences in inpatient mortality are more pronounced in patients with LLC than with CLI. Furthermore, regression analysis shows that sex is a significant predictor for patients diagnosed with LLC but not with CLI. Treatment guidelines should include consideration of sex in their indications for revascularization, particularly for patients diagnosed with LLC.

Small Bowel Adenocarcinoma as the Cause of Gastrointestinal Bleeding in Celiac Disease: A Rare Malignancy in a Common Disease.

Introduction. Celiac disease is associated with an increased risk of small bowel malignancies, particularly lymphoma. Its association with small bowel carcinoma is less known. Case Description. We report a case of an 89-year-old woman with celiac disease who experienced recurrent episodes of gastrointestinal bleeding and was ultimately found to have adenocarcinoma of the small intestine. Discussion and Evaluation. Diagnosis of small bowel adenocarcinoma is often delayed because of the need for specialized modalities, which are often deferred in the inpatient setting. Although resection is the modality of choice for small bowel tumors, a majority is either locally advanced or metastatic at diagnosis, and even localized cancers have worse prognosis than stage-matched colorectal tumors. The role of adjuvant chemotherapy is uncertain, but it is often offered extrapolating data from other gastrointestinal cancers. Small bowel carcinomas occurring in the context of celiac disease appear to be associated with higher rates of microsatellite instability than sporadic tumors, although other specific genomic abnormalities and mechanisms of carcinogenesis in celiac disease remain unknown. Conclusion. Recurrent episodes of gastrointestinal bleeding in a patient with celiac disease should prompt an early evaluation of the small bowel to assure timely diagnosis of carcinoma at an early curable stage.

Noise levels in a burn intensive care unit.

INTRODUCTION: Increased noise levels in hospitals, critical care units, and peri-operative areas have been associated with higher levels of sleep deprivation and patient stress. The World Health Organization (WHO) guidelines stipulate a limit of 35 decibels (dB(A)) equivalent continuous sound level (LEq) during the day and 30 dB(A) LEq at night in patients' rooms. To date, no quantitative studies of noise levels have been performed in burn units. The objective of this study was to quantify noise levels in a burn critical care unit to ascertain compliance with guidelines in order to minimize this potential insult. METHODS: An A-weighted sound pressure level meter was used to measure the ambient noise levels in a burn intensive care unit. Maximum and minimum sound pressure levels were measured at 30-min intervals on 10 days over a 1 month period. Measurements were obtained during shift changes and random times during the day and night-time. Descriptive statistical analyses were performed, to calculate means and standard deviations. Noise measurements at specified times were compared using analysis of variance (ANOVA). RESULTS: Mean dB(A) LEq values for shift changes, day, and night-time were 65.9 ± 2.8, 65.7 ± 2.6, and 60.9 ± 5.2 dB(A), respectively. There was no significant difference in dB(A)(max) or dB(A)(min) between shift changes, day or night-time (p>0.05). However, night-time minimum values were consistently lower. There was no significant difference between sound pressure level (SPL) inside and outside patients' rooms (p>0.05) at any time. CONCLUSIONS: Irrespective of time or location, the mean dB(A) LEq in the burn unit was significantly greater than World Health Organization (WHO), National Institute for Occupational Safety and Health (NIOSH), and the Environmental Protection Agency (EPA) recommendations. Guidelines for decreasing noise exposure are necessary to reduce potential negative effects on patients, visitors, and staff.

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Visceral artery aneurysms (VAA) and pseudoaneurysms (VAPA) can be life-threatening conditions with high incidence of rupture and hemorrhage. Greater availability and increased use of advanced imaging technology has led to the increased incidental detection of asymptomatic visceral aneurysms. In addition, increased percutaneous endovascular interventions have raised the incidence of iatrogenic pseudoaneurysms. Due to this, both VAA and VAPA have become an increasingly frequent diagnosis confronting the vascular surgeon. Over the past decade, there has been steady increase in the utilization of minimally invasive, non-operative interventions, for vascular occlusive and aneurysmal disease. All VAA and VAPA can technically be fixed by endovascular techniques but that does not mean they should. These catheter-based techniques constitute an excellent approach in the elective setting, particularly in patients who are poor surgical candidates due to their comorbidities or who present a hostile abdomen. However, in the emergent setting it may carry a higher morbidity and mortality. We review the literature about open and endovascular approach for the treatment of VAA and VAPA both in the elective and emergent setting.

Traumatic innominate artery pseudoaneurysm in the setting of a bovine arch.

Blunt traumatic injury of the innominate artery occurs infrequently but is commonly lethal. Bovine aortic arch anatomy is a predisposition to this injury. Clinical findings, chest X-ray, and computerized tomography may suggest the diagnosis, and it may be confirmed with angiography. Both interposition and bypass grafting are operative repair methods of choice. EEG monitoring confirms cerebral perfusion, thereby allowing the deferment of shunts and cardiovascular bypass with hypothermic arrest. We report a case of traumatic innominate artery pseudoaneurysm in the setting of "bovine aortic arch" anatomy, together with multiple associated injuries, including descending aorta transection. We also review the current literature on the topic.

Polyphenols are medicine: Is it time to prescribe red wine for our patients?

Alcohol, specifically red wine, has been suggested to play a key role in the prevention of cardiovascular disease and other chronic pathologies, including cancer. Its regular and moderate consumption has been found in numerous epidemiological studies to correlate inversely with vascular disease and mortality, despite the presence of risk factors such as high consumption of saturated fats, elevated smoking and low physical activity. This phenomenon, known as the 'French Paradox', would be explained mainly by the high levels of polyphenols present in red wine, making it more advantageous than beer, spirits and even white wine. The habit of having one or two drinks of red wine every day with meals may translate to a longer, healthier and better quality of life.

Differential effects of shear stress and cyclic strain on Sp1 phosphorylation by protein kinase Czeta modulates membrane type 1-matrix metalloproteinase in endothelial cells.

Membrane type 1-matrix metalloproteinase (MT1-MMP) plays a key role in extracellular matrix remodeling, endothelial cell (EC) migration, and angiogenesis. Whereas cyclic strain (CS) increases MT1-MMP expression, shear stress (SS) decreases MT1-MMP expression. The aim of this study was to determine if changes in levels of Sp1 phosphorylation induced by protein kinase Czeta (PKCzeta) in ECs exposed to SS but not CS are important for MT1-MMP expression. The results showed that SS increased Sp1 phosphorylation, which could be inhibited by pretreatment with PKCzeta inhibitors. In the presence of PKCzeta inhibitors, the SS-mediated decrease in MT1-MMP protein expression was also abolished. These data demonstrate that increased affinity of Sp1 for MT1-MMP's promoter site occurs as a consequence of PKCzeta-induced phosphorylation of Sp1 in response to SS, increasing Sp1 binding affinity for the promoter site, preventing Egr-1 binding, and consequently decreasing MT1-MMP expression.

Resveratrol inhibits vascular smooth muscle cell proliferation and induces apoptosis.

OBJECTIVE: In France, despite a high intake of dietary cholesterol and saturated fat, the cardiovascular death rate is one of the lowest among developed countries. This "French paradox" has been postulated to be related to the high red wine intake in France. The aim of this study was to determine the effects of resveratrol, a major polyphenol component of red wine, on vascular smooth muscle cell (SMC) proliferation in vitro. METHODS: SMCs were exposed to 10(-6) to 10(-4) M resveratrol and cell proliferation was assessed by cell counting. Cell cycle analysis was done by treating cells with propidium iodide followed by flow-activated cell sorting. Apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling staining. RESULTS: We demonstrate that resveratrol inhibited bovine aortic SMC proliferation in a dose-dependent manner. The lowest concentration of resveratrol resulting in a significant decrease in SMC proliferation compared with control was 10(-5) M. By flow cytometry, we observed a block in the G1-S phase of the SMC cycle. Resveratrol treatment also resulted in a dose-dependent apoptosis of SMCs but had no effects on SMC morphology. CONCLUSION: The results indicated that vascular SMC proliferation could be inhibited by resveratrol through a block on G1-S phase and by an increase in apoptosis. It supports the conjecture that red wine consumption may have a beneficial effect on cardiovascular mortality. CLINICAL RELEVANCE: Our results suggest that resveratrol inhibits, in a dose-dependent manner, smooth muscle cell proliferation, which may help to partially explain a beneficial effect of wine drinking. This inhibition is related to an early block in the cell cycle and also to a dose-dependent apoptotic effect. The present study demonstrates that resveratrol not only is an indirect marker of a healthy life style and alimentation but may also be directly responsible for the French paradox.

MAPKs (ERK1/2, p38) and AKT can be phosphorylated by shear stress independently of platelet endothelial cell adhesion molecule-1 (CD31) in vascular endothelial cells.

PECAM-1 (CD31) is a member of the Ig superfamily of cell adhesion molecules and is expressed on endothelial cells (EC) as several circulating blood elements including platelets, polymorphonuclear leukocytes, monocytes, and lymphocytes. PECAM-1 tyrosine phosphorylation has been observed following mechanical stimulation of EC but its role in mechanosensing is still incompletely understood. The aim of this study was to investigate the involvement of PECAM-1 in signaling cascades in response to fluid shear stress (SS) in vascular ECs. PECAM-1-deficient (KO) and PECAM-reconstituted murine microvascular ECs, 50 and 100% confluent bovine aortic EC (BAEC), and human umbilical vein EC (HUVEC) transfected with antisense PECAM-1 oligonucleotides were exposed to oscillatory SS (14 dynes/cm2) for 0, 5, 10, 30 or 60 min. The tyrosine phosphorylation level of PECAM-1 immunoprecipitated from SS-stimulated PECAM-reconstituted, but not PECAM-1-KO, murine ECs increased. Although PECAM-1 was phosphorylated in 100% confluent BAEC and HUVEC, its phosphorylation level in 50% confluent BAECs or HUVEC was not detected by SS. Likewise PECAM-1 phosphorylation was robust in the wild type and scrambled-transfected HUVEC but not in the PECAM-1 antisense-HUVEC. ERK(1/2), p38 MAPK, and AKT were activated by SS in all cell types tested, including the PECAM-1-KO murine ECs, 50% confluent BAECs, and HUVEC transfected with antisense PECAM-1. This suggests that PECAM-1 may not function as a major mechanoreceptor for activation of MAPK and AKT in ECs and that there are likely to be other mechanoreceptors in ECs functioning to detect shear stress and trigger intercellular signals.