Risk factors for superficial surgical site infection after elective rectal cancer resection: a multivariate analysis of 8880 patients from the American College of Surgeons National Surgical Quality Improvement Program database.

BACKGROUND: Superficial surgical site infection (sSSI) is one of the most common complications after colorectal resection. The goal of this study was to determine the comorbidities and operative characteristics that place patients at risk for sSSI in patients who underwent rectal cancer resection. METHODS: The American College of Surgeons National Surgical Quality Improvement Program database was queried (via diagnosis and Current Procedural Terminology codes) for patients with rectal cancer who underwent elective resection between 2005 and 2012. Patients for whom data concerning 27 demographic factors, comorbidities, and operative characteristics were available were eligible. A univariate and multivariate analysis was performed to identify possible risk factors for sSSI. RESULTS: A total of 8880 patients met the entry criteria and were included. sSSIs were diagnosed in 861 (9.7%) patients. Univariate analysis found 14 patients statistically significant risk factors for sSSI. Multivariate analysis revealed the following risk factors: male gender, body mass index (BMI) >30, current smoking, history of chronic obstructive pulmonary disease (COPD), American Society of Anesthesiologists III/IV, abdominoperineal resection (APR), stoma formation, open surgery (versus laparoscopic), and operative time >217 min. The greatest difference in sSSI rates was noted in patients with COPD (18.9 versus 9.5%). Of note, 54.2% of sSSIs was noted after hospital discharge. With regard to the timing of presentation, univariate analysis revealed a statistically significant delay in sSSI presentation in patients with the following factors and/or characteristics: BMI <30, previous radiation therapy (RT), APR, minimally invasive surgery, and stoma formation. Multivariate analysis suggested that only laparoscopic surgery (versus open) and preoperative RT were risk factors for delay. CONCLUSIONS: Rectal cancer resections are associated with a high incidence of sSSIs, over half of which are noted after discharge. Nine patient and operative characteristics, including smoking, BMI, COPD, APR, and open surgery were found to be significant risk factors for SSI on multivariate analysis. Furthermore, sSSI presentation in patients who had laparoscopic surgery and those who had preoperative RT is significantly delayed for unclear reasons.

Role of Minimally Invasive Surgery in the Reoperative Abdomen or Pelvis.

Laparoscopy has become widely accepted as the preferred surgical approach in the management of benign and malignant colorectal diseases. Once considered a relative contraindication in patients with prior abdominal surgery (PAS), as surgeons have continued to gain expertise in advanced laparoscopy, minimally invasive approaches have been increasingly incorporated in the reoperative abdomen and pelvis. Although earlier studies have described conversion rates, most contemporary series evaluating the impact of PAS in laparoscopic colorectal resection have reported equivalent conversion and morbidity rates between reoperative and non-reoperative cases, and series evaluating the impact of laparoscopy in reoperative cases have demonstrated improved short-term outcomes with laparoscopy. The data overall highlight the importance of case selection, careful preoperative preparation and planning, and the critical role of surgeons' expertise in advanced laparoscopic techniques. Challenges to the widespread adoption of minimally invasive techniques in reoperative colorectal cases include the longer learning curve and longer operative time. However, with the steady increase in adoption of minimally invasive techniques worldwide, minimally invasive surgery (MIS) is likely to continue to be applied in the management of increasingly complex reoperative colorectal cases in an effort to improve patient outcomes. In the hands of experienced MIS surgeons and in carefully selected cases, laparoscopy is both safe and efficacious for reoperative procedures in the abdomen and pelvis, with measurable short-term benefits.

Arterial shear stress reduces eph-b4 expression in adult human veins.

Vein graft adaptation to the arterial environment is characterized by loss of venous identity, with reduced Ephrin type-B receptor 4 (Eph-B4) expression but without increased Ephrin-B2 expression. We examined changes of vessel identity of human saphenous veins in a flow circuit in which shear stress could be precisely controlled. Medium circulated at arterial or venous magnitudes of laminar shear stress for 24 hours; histologic, protein, and RNA analyses of vein segments were performed. Vein endothelium remained viable and functional, with platelet endothelial cell adhesion molecule (PECAM)-expressing cells on the luminal surface. Venous Eph-B4 expression diminished (p = .002), Ephrin-B2 expression was not induced (p = .268), and expression of osteopontin (p = .002) was increased with exposure to arterial magnitudes of shear stress. Similar changes were not found in veins placed under venous flow or static conditions. These data show that human saphenous veins remain viable during ex vivo application of shear stress in a bioreactor, without loss of the venous endothelium. Arterial magnitudes of shear stress cause loss of venous identity without gain of arterial identity in human veins perfused ex vivo. Shear stress alone, without immunologic or hormonal influence, is capable of inducing changes in vessel identity and, specifically, loss of venous identity.

Reduced adult endothelial cell EphB4 function promotes venous remodeling.

Reduced EphB4 expression is observed during vein graft adaptation and is associated with increased venous wall thickening. These findings suggest that EphB4 may mediate normal adult venous endothelial cell (EC) function and vein graft adaptation. We therefore tested the functional significance of EphB4 using EC with genetically reduced EphB4 signaling. EC were isolated from EphB4(+/+) and EphB4(+/-) mice. In vitro function was assessed through EC proliferation, migration, nitric oxide (NO) synthesis, and chemokine production. A mouse vein graft model was used to correlate in vitro findings with in vivo vein grafts. Smooth muscle cells (SMC) were subjected to proliferation and migration assays using EphB4(+/+) and EphB4(+/-) EC-conditioned medium. EphB4(+/-) EC exhibited diminished proliferation (P < 0.0001, n = 6), migration (P < 0.0001, n = 3), and NO production (P = 0.0012, n = 3). EphB4(+/-) EC had increased VEGF-A mRNA (P = 0.0006, n = 6) and protein (P = 0.0106, n = 3) as well as increased secretion of VEGF-A (P = 0.0010, n = 5), PDGF-BB (P < 0.0001, n = 6), and TGF-ß1 (P < 0.0001, n = 6). EphB4(+/-)-conditioned medium promoted SMC proliferation (P < 0.0001, n = 7) and migration (P = 0.0358, n = 3). Vein grafts and EphB4(+/-) EC showed similarity with regard to VEGF-A and eNOS mRNA and protein expression. In conclusion, reduced venous EC EphB4 function is associated with a proangiogenic and mitogenic phenotype. EphB4(+/-) EC have increased secretion of SMC mitogens and reduced NO production that correlate with the thickened neointima formed during vein graft adaptation. These findings suggest that EphB4 remains active in adult venous EC and that loss of EphB4 plays a role in vein graft adaptation.

Eph-B4 prevents venous adaptive remodeling in the adult arterial environment.

Eph-B4 determines mammalian venous differentiation in the embryo but is thought to be a quiescent marker of adult veins. We have previously shown that surgical transposition of a vein into the arterial environment is characterized by loss of venous identity, as indicated by the loss of Eph-B4, and intimal thickening. We used a mouse model of vein graft implantation to test the hypothesis that Eph-B4 is a critical determinant of venous wall thickness during postsurgical adaptation to the arterial environment. We show that stimulation of Eph-B4 signaling, either via ligand stimulation or expression of a constitutively active Eph-B4, inhibits venous wall thickening and preserves venous identity; conversely, reduction of Eph-B4 signaling is associated with increased venous wall thickness. Stimulated Eph-B4 associates with caveolin-1 (Cav-1); loss of Cav-1 or Eph-B4 kinase function abolishes inhibition of vein graft thickening. These results show that Eph-B4 is active in adult veins and regulates venous remodeling. Eph-B4-Cav-1-mediated vessel remodeling may be a venous-specific adaptive mechanism. Controlled stimulation of embryonic signaling pathways such as Eph-B4 may be a novel strategy to manipulate venous wall remodeling in adults.

Venous and arterial identity: a role for caveolae?

Venous and arterial identity is predetermined in the embryo, with embryonic vessels expressing Eph-B4 differentiating into veins and vessels expressing ephrin-B2 differentiating into arteries. The specialized membrane organelles lipid rafts and caveolae serve as localized domains for proteins to interact with one another and play a role in signal transduction and vesicular trafficking. Several tyrosine kinase membrane receptors, including Eph-B1, have been colocalized to caveolae. These data suggest that caveolae and Eph receptors may have coordinated roles in determining vessel identity, not only during embryogenesis but perhaps also during adult vascular remodeling and angiogenesis.