Chylous leakage after esophagectomy for esophageal cancer: a systematic review.

BACKGROUND: Chylous leakage is a rare complication following esophagectomy; however, it can lead to mortality. We aimed to systematically evaluate the factors that may lead to increased chylous leakage after esophagectomy. METHODS: Three databases (PubMed, Embase, and Cochrane Library) were systematically searched for all studies investigating the occurrence of chylous leakage after esophagectomy. RESULTS: A total of 32 studies were identified, including 26 randomized controlled trials and 3 cohort and case-control studies, each. The overall incidence of chylous leakage was 4.7% (278/5,971 cases). Analysis of preoperative, intraoperative, and postoperative factors showed that most of the qualitative analysis results did not significantly increase the incidence of chylous leakage. In some quantitative analyses, the chylous leakage rate was significantly lower in the thoracic duct mass ligation group than in the conservative treatment group (relative risk [RR] = 0.33; 95% confidence interval [CI], 0.13-0.83; I2 = 0.0%; P = 0.327). Direct oral feeding significantly reduced chylous leakage compared with jejunostomy (RR = 0.06; 95% CI 0.01-0.33; I2 = 0.0%; P = 0.335). However, preoperative inspiratory muscle training (RR = 1.66; 95% CI, 0.21-12.33; I2 = 55.5%; P = 0.134), preoperative chemoradiotherapy (RR = 0.99; 95% CI, 0.55-1.80; I2 = 0.0%; P = 0.943), and robotic assistance (RR = 1.62; 95% CI, 0.92-2.86; I2 = 0.0%; P = 0.814) did not significantly reduce the incidence of chylous leakage. CONCLUSIONS: Ligation of the thoracic duct and direct oral feeding can reduce the incidence of chylous leakage after esophagectomy in patients with esophageal cancer. Other contributing factors remain unclear and require validation in further high-quality studies.

Inducible nitric oxide synthase activity mediates TNF-α-induced endothelial cell dysfunction.

Inducible nitric oxide synthase (iNOS) and vascular endothelial dysfunction have been implicated in the development and progression of atherosclerosis. This study aimed to elucidate the role of iNOS in vascular endothelial dysfunction. Ultrahigh performance liquid chromatography-quadrupole time-of-flight mass spectrometry combined with multivariate data analysis was used to characterize the metabolic changes in human umbilical vein endothelial cells (HUVECs) in response to different treatment conditions. In addition, molecular biology techniques were employed to explain the molecular mechanisms underlying the role of iNOS in vascular endothelial dysfunction. Tumor necrosis factor-α (TNF-α) enhances the expression of iNOS, TXNIP, and the level of reactive oxygen species (ROS) facilitates the entry of nuclear factor-κB (NF-κB) into the nucleus and promotes injury in HUVECs. iNOS deficiency reversed the TNF-α-mediated pathological changes in HUVECs. Moreover, TNF-α increased the expression of tumor necrosis factor receptor-2 (TNFR-2) and the levels of p-IκBα and IL-6 proteins and CD31, ICAM-1, and VCAM-1 protein expression, which was significantly reduced in HUVECs with iNOS deficiency. In addition, treating HUVECs in the absence or presence of TNF-α or iNOS, respectively, enabled the identification of putative endogenous biomarkers associated with endothelial dysfunction. These biomarkers were involved in critical metabolic pathways, including glycosylphosphatidylinositol-anchor biosynthesis, amino acid metabolism, sphingolipid metabolism, and fatty acid metabolism. iNOS deficiency during vascular endothelial dysfunction may affect the expression of TNFR-2, vascular adhesion factors, and the level of ROS via cellular metabolic changes, thereby attenuating vascular endothelial dysfunction.NEW & NOTEWORTHY Inducible nitric oxide synthase (iNOS) deficiency during vascular endothelial dysfunction may affect the expression of tumor necrosis factor receptor-2 and vascular adhesion factors via cellular metabolic changes, thereby attenuating vascular endothelial dysfunction.

The clinical effectiveness of wound edge protectors in reducing surgical site infection after abdominal surgery: meta-analysis.

BACKGROUND: Surgical site infection (SSI) is a common complication after abdominal surgery. The effectiveness of wound edge protectors in reducing infection of the surgical sites is still unclear. The purpose of this study was to determine the clinical effectiveness of a wound edge protector (WEP) in reducing SSI rates after abdominal surgery. METHODS: PubMed, Embase, Web of Science, and the Cochrane Library were systematically searched to obtain relevant articles published up to September 2021. Publications were retrieved if they contain primary data on the use of WEPs in reducing SSI compared with standard care in patients undergoing abdominal surgery. Subgroup analyses were performed for different WEP types, surgical sites, and levels of contamination. The outcome of interest was a clinically defined SSI. Qualitative variables were pooled using risk ratios (RRs). RESULTS: Twenty-two eligible randomized clinical trials involving 4492 patients were included in this meta-analysis. WEP was associated with the reduced incidence of overall SSI (RR = 0.66; 95 per cent c.i. 0.53 to 0.83; P = 0.0003), and superficial SSI (RR = 0.59; 95 per cent c.i. 0.38 to 0.91; P = 0.02). In addition, WEP also successfully reduced the risk of SSI in clean-contaminated wounds (RR = 0.61; 95 per cent c.i. 0.40 to 0.93; P = 0.02) as well as in contaminated wounds (RR = 0.47; 95 per cent c.i. 0.33 to 0.67; P < 0.0001); however, WEP did not reduce SSI incidence in colorectal surgery (RR = 0.68; 95 per cent c.i. 0.46 to 1.01; P = 0.05). CONCLUSION: This study suggests that WEP was efficient in reducing superficial SSI. Both double-ringed and single-ringed devices were efficient in reducing SSI. WEP was effective in reducing SSI incidence in clean-contaminated and contaminated surgery; however, its use does not reduce the SSI rate in colorectal surgery.