Association of socioeconomic status with 30- and 90-day readmission following open and laparoscopic hernia repair: a nationwide readmissions database analysis.

BACKGROUND: Socioeconomic disparities have been associated with outcomes in many medical conditions. The association of socioeconomic status (SES) with readmissions after ventral and inguinal hernia repair has not been well studied on a national level. This study aims to evaluate the association of SES with readmission as a significant outcome in patients undergoing ventral and inguinal hernia repair. METHODS: A retrospective cohort study was performed evaluating patients undergoing ventral hernia and inguinal hernia repair with 1:1 propensity score matching using the Nationwide Readmissions Database (2016-2017). Both 30- and 90-day readmissions were examined. After matching, a multivariate logistic regression analysis was performed using confounding variables including hospital setting, comorbidities, urgency of repair, sociodemographic status, and payer. Likelihood of readmission was reported in odds ratio form. RESULTS: Readmission rates were 11.56% (24,323 out of 210,381) and 17.94% (30,893 out of 172,210) for 30- and 90-day readmissions, respectively. Patients with Medicaid and in the lower income quartile were more likely to present in an emergent fashion for hernia repair. After matching, a multivariate logistic regression analysis showed socioeconomic status (OR 1.250 and 1.229) was a statistically significant independent predictor of readmission at 30 and 90 days, respectively. Inversely, factors associated with the least likely chance of readmission were a laparoscopic approach (OR 0.646 and 0.641), elective admission (OR 0.824 and 0.779), and care in a teaching hospital (OR 0.784 and 0.798). CONCLUSION: SES is an independent predictor of readmission at 30 and 90 days following open and laparoscopic ventral and inguinal hernia repair. Patients with a lower socioeconomic status were more likely to undergo hernia repair in the emergent setting. Efforts toward mitigating SES disparities by potentially promoting MIS techniques, enhancing access to elective cases, and systematic approaches to perioperative care for this disadvantaged population can potentially enhance overall hernia outcomes.

Lower Gastrointestinal Bleeding.

Lower gastrointestinal bleeding entails a range of severity and a multitude of options for localization and control of bleeding. With experience in trauma, critical care, endoscopy, and definitive surgical interventions, general surgeons are equipped to manage this condition in various clinical settings. This article examines traditional and emerging options for bleeding localization and control available to general surgeons.

Utility of clinical decision rule for intensive care unit admission in patients with traumatic intracranial hemorrhage.

BACKGROUND: Recent literature suggests the majority of traumatic intracranial hemorrhage does not require intervention. One recently described clinical decision rule was sensitive in identifying patients requiring critical care interventions in an urban setting. We sought to validate its effectiveness in our predominately rural setting. METHODS: A retrospective study was conducted of adult patients with traumatic intracranial hemorrhage. The rule, based on age, initial Glasgow coma scale score, and presence of a non-isolated head injury, was applied to externally validate the previously reported findings. RESULTS: In our population, the rule displayed a sensitivity of 0.923, specificity of 0.251, positive predictive value of 0.393, and negative predictive value of 0.862. The area under curve was 0.587. While our population has a similar adjusted head injury severity score as that from which the rule was developed, significant differences in age and intracranial hemorrhage pattern were noted. CONCLUSIONS: The rule displayed decreased performance in our population, most likely secondary to differences in age and intracranial hemorrhage patterns. Prospective evaluation and cost-savings analysis are appropriate subsequent steps for the rule.

Anti-VEGF-A therapy reduces lymphatic vessel density and expression of VEGFR-3 in an orthotopic breast tumor model.

Because metastasis contributes significantly to cancer mortality, understanding its mechanisms is crucial to developing effective therapy. Metastasis is facilitated by lymphangiogenesis, the growth of new intratumoral or peritumoral lymphatic vessels from pre-existing vessels. Vascular endothelial growth factor A (VEGF-A) is a well-known angiogenic factor. Increasing evidence implicates VEGF-A in lymphangiogenesis, although the mechanism of its pro-lymphangiogenic effect is poorly understood. We examined the effect of the anti-VEGF-A neutralizing antibody 2C3 on tumor lymphangiogenesis and metastasis in an orthotopic breast carcinoma model using MDA-MB-231 cells and its luciferase-tagged derivative, 231-Luc(+) cells. Anti-VEGF-A antibody therapy reduced blood and lymphatic vessel densities by 70% and 80%, respectively, compared with the control antibody. Treatment with 2C3 antibody also decreased incidence of lymphatic and pulmonary metastases by 3.2- and 4.5-fold, respectively. Macrophage infiltration was reduced in 2C3-treated tumors by 32%, but VEGF-C expression was unchanged. In contrast, neoplastic cells and blood vessels in tumors from 2C3-treated mice expressed significantly less angiopoietin-2 (Ang-2) than tumors from control mice. The reduction in Ang-2 was associated with inhibition of VEGFR-3 expression in intratumoral lymphatic endothelial cells. Both VEGF-A and Ang-2 upregulated the expression of VEGFR-3 in cultured lymphatic endothelial cells. VEGF-A induced proliferation of lymphatic endothelial cells was reduced by 50% by soluble Tie-2, suggesting that Ang-2 is an intermediary of the pro-lymphangiogenic VEGF-A effect. These results suggest a novel mechanism by which anti-VEGF-A therapy may suppress tumor lymphangiogenesis and subsequent metastasis supporting the use of anti-VEGF-A therapy to control metastasis clinically.

Molecular profile and proliferative responses of rat lymphatic endothelial cells in culture.

BACKGROUND: Lymphangiogenesis plays an important role in metastasis of many solid tumors. To study lymphangiogenesis under controlled conditions, an in vitro model is needed. The goal of this work was to establish such an in vitro model by determining a molecular profile of rat mesenteric lymphatic endothelial cells (RMLEC) and characterizing their proliferative responses to angiogenic and lymphangiogenic factors, such as vascular endothelial growth factor A and C (VEGF-A and VEGF-C). METHODS AND RESULTS: RMLEC strongly expressed most lymphatic-specific markers, including Prox-1, LYVE-1, and VEGFR-3. Proliferation of RMLEC was serum and heparin dependent. In the presence of low (2%) serum concentration, exogenously added VEGF-A and VEGFC stimulated RMLEC in a linear and dose-dependent manner. This effect was abrogated by anti-VEGF-A and VEGF-C antibodies, as well as by soluble Tie-2 and Flt-4 fusion proteins. Abrogation was reversed by VEGF-A, suggesting that this factor as an important regulator of lymphangiogenesis. CONCLUSIONS: Cultured RMLEC preserved a molecular profile consistent with the phenotype of lymphatic endothelium in vivo and respond to either VEGF-A or VEGF-C factors. VEGFA was able to rescue RMLEC proliferation inhibited by a neutralizing VEGF-C antibody or soluble Tie-2 fusion protein. These results support the existence of cross-talk among angiogenic and lymphangiogenic factors. This work established experimental conditions that allow in vitro modeling of lymphatic endothelial responses to lymphangiogenic regulators. Preliminary results using this model suggest that VEGF-A, VEGF-C, and angiopoietins work in concert to promote lymphangiogenesis in vivo.