Incidence and predictors of case cancellation within 24 h in patients scheduled for elective surgical procedures.

OBJECTIVE: Avoidable case cancellations within 24 h reduce operating room (OR) efficiency, add unnecessary costs, and may have physical and emotional consequences for patients and their families. We developed and validated a prediction tool that can be used to guide same day case cancellation reduction initiatives. DESIGN: Retrospective hospital registry study. SETTING: University-affiliated hospitals network (NY, USA). PATIENTS: 246,612 (1/2016-6/2021) and 58,662 (7/2021-6/2022) scheduled elective procedures were included in the development and validation cohort. MEASUREMENTS: Case cancellation within 24 h was defined as cancelling a surgical procedure within 24 h of the scheduled date and time. Our candidate predictors were defined a priori and included patient-, procedural-, and appointment-related factors. We created a prediction tool using backward stepwise logistic regression to predict case cancellation within 24 h. The model was subsequently recalibrated and validated in a cohort of patients who were recently scheduled for surgery. MAIN RESULTS: 8.6% and 8.7% scheduled procedures were cancelled within 24 h of the intended procedure in the development and validation cohort, respectively. The final weighted score contains 29 predictors. A cutoff value of 15 score points predicted a 10.3% case cancellation rate with a negative predictive value of 0.96, and a positive predictive value of 0.21. The prediction model showed good discrimination in the development and validation cohort with an area under the receiver operating characteristic curve (AUC) of 0.79 (95% confidence interval 0.79-0. 80) and an AUC of 0.73 (95% confidence interval 0.72-0.73), respectively. CONCLUSIONS: We present a validated preoperative prediction tool for case cancellation within 24 h of surgery. We utilize the instrument in our institution to identify patients with high risk of case cancellation. We describe a process for recalibration such that other institutions can also use the score to guide same day case cancellation reduction initiatives.

Examining intersectionality in anesthesiology training, academics, and practice.

PURPOSE OF REVIEW: Intersectionality, or the overlapping nature of social categorizations, such as race, class, and gender, creates interdependent systems of discrimination, disadvantage, and health disparities. The present review examines common shortcomings to diversity management, and proposes targeted improvement frameworks for anesthesiology departments that would offer competitive advantage in training, hiring, and retention, and improved care delivery aimed toward reducing health disparities. RECENT FINDINGS: Studies highlight that physicians equipped to care for diverse populations enhance patient-doctor interactions and reduce health disparities. Moreover, untrained providers and staff who engage in disrespectful behaviors like microaggressions can lead to staff turnover and millions of dollars in lost revenue. Underrepresented minorities continue to have lower faculty academic rank in anesthesiology, fewer partnership opportunities in private practice, and disparate research funding. Diversity-based education and training often overlooks intersectionality and reductively illustrates diverse groups as internally homogenous. Even these developing diversity efforts have become politicized and are perceived as uninteresting, irrelevant to medical practice, or unable to create organizational change. SUMMARY: The synergy of intersectionality mounts considerable challenges that impact patients, colleagues, and communities of practice. Examining intersectionality in education and workplace policy affords tremendous opportunity for improving quality of care for marginalized populations, reducing healthcare costs, and normalizing culture that is inclusive, equitable, and empowering.

Professionalism: microaggression in the healthcare setting.

PURPOSE OF REVIEW: Microaggressions are daily commonplace, subtle behaviors and attitudes toward others that arise from conscious or unconscious bias. Not only can microaggressions affect one's access to power, resources, and opportunity, but they could also contribute to the persistent disparities faced by marginalized groups among healthcare professionals as well as patients. RECENT FINDINGS: Physicians, especially those in perioperative specialties, commonly have distress during their medical training. Workplace mistreatment, such as discrimination, has been commonly reported by residents across multiple specialties. Microaggressions also impact patient care as they can influence decisions of medical professionals toward a person or group of people. SUMMARY: This review offers education on the correlation of microaggression and unconscious bias to health disparities, provides tools to address microaggressions as a bystander, and outlines processes for institutional improvement.

Endothelin type A receptor blockade reduces vascular calcification and inflammation in rats with chronic kidney disease.

OBJECTIVE: Arterial stiffness and calcification are nontraditional cardiovascular risk factors in chronic kidney disease (CKD). Using a rat model of CKD with mineral imbalance, medial vascular calcification has been associated with inflammation and increased endothelin-1 (ET-1) production. We therefore hypothesized that ET-1, through the endothelin type A (ETA) receptor, induces vascular inflammation, calcification and stiffness in CKD. METHODS: CKD was induced in Wistar rats by renal mass ablation. To induce medial vascular calcification, mineral imbalance was established with a identified as calcium-rich/phosphate-rich diet and vitamin D supplementation (Ca/P/VitD). One group of CKD + Ca/P/VitD rats was given the ETA receptor antagonist atrasentan (10 mg/kg/day) for 6 weeks. Hemodynamic parameters including SBP, pulse pressure (PP) and pulse wave velocity (PWV) were determined. Vascular calcification, smooth muscle cells osteoblastic differentiation and expression of inflammatory markers such as inflammatory cytokines and calgranulins S100A8 and S100A9 were assessed in the thoracic aorta. RESULTS: As compared with CKD control rats, CKD + Ca/P/VitD rats developed medal vascular calcification that was associated with increased SBP, PP and PWV. These changes were also associated with increased macrophage infiltration and expression of IL-6, calgranulins and osteoblastic markers. Treatment of CKD + Ca/P/VitD rats with atrasentan reduced vascular calcification, SBP, PP and PWV, macrophage infiltration and expression of IL-1ß, IL-6, tumor necrosis factor, calgranulins and osteoblastic markers. CONCLUSION: This study shows that ETA receptor blockade reduced vascular inflammation, smooth muscle cells differentiation, calcification and stiffness indicating a pivotal role for ET-1 in medial vascular calcification in this rat remnant kidney model of CKD with mineral imbalance. Therefore, the endothelin system may be a potential therapeutic target for improving cardiovascular morbidity in patients with CKD.

Inflammatory cytokines and reactive oxygen species as mediators of chronic kidney disease-related vascular calcification.

BACKGROUND: Vascular calcification, a regulated process in chronic kidney disease (CKD), requires vascular smooth muscle cell (VSMC) differentiation into osteoblast-like cells. This phenomenon can be enhanced by inflammatory cytokines and production of reactive oxygen species (ROS). In CKD rats with vascular calcification, we investigated whether inflammatory cytokines, ROS generation, and downstream signaling events are associated with CKD-related vascular calcification. METHODS: CKD was induced in male Wistar rats by renal mass ablation and vascular calcification was induced with a high calcium-phosphate diet and vitamin D supplementation (Ca/P/VitD). At week 3-6, hemodynamic parameters were determined and thoracic aorta was harvested for assessment of vascular calcification, macrophage infiltration, cytokines expression, VSMC differentiation, ROS generation, and related signaling pathway activation. RESULTS: CKD rats treated with Ca/P/VitD developed medial calcification of thoracic aorta and increased pulse pressure and aortic pulse wave velocity. VSMC differentiation was confirmed by increased bone morphogenetic protein-2 and osteocalcin expression and reduced α-smooth muscle actin expression. The expression of interleukin-1ß, interleukin-6, and tumor necrosis factor were also increased. The expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits p22(phox) and p47(phox) were increased, whereas the expression of antioxidant enzymes (SOD1, SOD2, Gpx1, and Prdx1) was reduced in CKD + Ca/P/VitD rats. Oxidized peroxiredoxin, a sensor of ROS generation, was significantly increased and ROS-sensitive signaling pathways were activated in the aorta from CKD + Ca/P/VitD rats. CONCLUSION: This study demonstrates a relationship between inflammation/ROS and arterial calcification in CKD and contributes to understanding of the complex pathways that mediate arterial calcification in CKD patients.

Vascular remodeling and media calcification increases arterial stiffness in chronic kidney disease.

BACKGROUND: Cardiovascular disease is the most common cause of death in patients with chronic kidney disease (CKD). Arterial stiffness and calcification are non-traditional risk factors of cardiovascular disease in CKD. In CKD rats, we investigated the involvement of smooth muscle cells differentiation to osteoblast-like cells and blood vessel wall remodeling, associated with media calcification, in arterial stiffness. METHOD: CKD with vascular calcification was induced by subtotal nephrectomy followed by treatment with a high calcium and phosphate diet, and vitamin D supplementation (Ca/P/VitD). At week 3-6, hemodynamic parameters and pulse wave velocity (PWV) were assessed. Vascular media calcification and remodeling were determined by histological von Kossa staining and confocal immunofluorescence analysis of osteocalcin, elastin, α-smooth muscle actin (α-SMA) and collagen-1. RESULTS: Treatment of CKD rats with Ca/P/VitD, but not normal animals, induced a significant increase in pulse pressure and PWV (p < 0.05) and marked calcification in the media. In calcification areas, de novo expression of osteocalcin was observed, whereas α-SMA immunofluorescence levels were reduced (p < 0.01). The immunofluorescence levels of elastin were also reduced, which was related to disruption of elastic lamella. In contrast, collagen-1 immunofluorescence levels in areas of calcification were increased (p < 0.01). Changes in both α-SMA and elastin inversely correlated with the PWV. CONCLUSION: This study indicate that smooth muscle cells differentiation to osteoblast-like cells and the associated media remodeling, which includes disruption of elastic lamellas and deposition of collagen are, at least in part, associated with the increased arterial stiffness observed in CKD rats with vascular calcification.

General anesthesia and methylenetetrahydrofolate reductase deficiency.

Methylenetetrahydrofolate reductase (MTHFR) deficiency is an autosomal recessive disorder with a spectrum of manifestations including neurological symptoms, premature arteriosclerosis, and venous and arterial thrombosis. Most patients are heterozygous for multiple MTHFR substitutions; small minorities are homozygous for mutations at this locus. Among these mutations, the C677T polymorphism is the most deleterious. Nitrous oxide use in anesthesia leads to significant increases in plasma homocysteine. We present a patient undergoing urgent surgery with a preoperative diagnosis of homozygous MTHFR deficiency.