Vasculink iPhone Application and Risk Prediction Model for Groin Complication in Vascular Surgery.

BACKGROUND: Postoperative groin complication is a common cause of morbidity in vascular surgery. Prophylactic wound adjuncts addressing this issue have been shown to reduce complications in high-risk patients, but their widespread implementation is limited by their high cost. This study introduces a risk prediction model for patients at a high risk for groin complication which can be accessed through the iPhone application, Vasculink. METHODS: A literature search identified risk prediction models for groin complication in vascular surgery. Odds ratios of risk factors that were present in at least 2 published models were calculated with a pooled effect size. The weighted risk for each factor was used to create our model and a cutoff point defining high risk patients was chosen. The initial model was assessed and validated using a split-sample methodology on a cohort identified via a retrospective chart review of all patients undergoing open vascular surgery at our institution between 2017 and 2020. Model performance was assessed using the C-statistic. RESULTS: Risk factors included in our model were female gender, body mass index ≥28 kg/m2, ever-smoker, reoperation, use of prosthetic, emergency, and end-stage renal disease. Of 216 patients, 131 were at a high risk. The overall groin complication rate was 43%, and specific complication rates were 27% infection, 14.8% seroma, and 6.9% hematoma. Our model's sensitivity and specificity were 92.47% and 60.98%, respectively. The C-statistic is 0.768. CONCLUSIONS: By using risk factors identified in the literature we have been able to establish a highly sensitive risk prediction model for groin complication following open vascular surgery. By incorporating our model into an iPhone application, Vasculink, we hope to facilitate preoperative decision making regarding the use of prophylactic wound adjuncts.

Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver.

Mitochondria are critical for respiration in all tissues; however, in liver, these organelles also accommodate high-capacity anaplerotic/cataplerotic pathways that are essential to gluconeogenesis and other biosynthetic activities. During nonalcoholic fatty liver disease (NAFLD), mitochondria also produce ROS that damage hepatocytes, trigger inflammation, and contribute to insulin resistance. Here, we provide several lines of evidence indicating that induction of biosynthesis through hepatic anaplerotic/cataplerotic pathways is energetically backed by elevated oxidative metabolism and hence contributes to oxidative stress and inflammation during NAFLD. First, in murine livers, elevation of fatty acid delivery not only induced oxidative metabolism, but also amplified anaplerosis/cataplerosis and caused a proportional rise in oxidative stress and inflammation. Second, loss of anaplerosis/cataplerosis via genetic knockdown of phosphoenolpyruvate carboxykinase 1 (Pck1) prevented fatty acid-induced rise in oxidative flux, oxidative stress, and inflammation. Flux appeared to be regulated by redox state, energy charge, and metabolite concentration, which may also amplify antioxidant pathways. Third, preventing elevated oxidative metabolism with metformin also normalized hepatic anaplerosis/cataplerosis and reduced markers of inflammation. Finally, independent histological grades in human NAFLD biopsies were proportional to oxidative flux. Thus, hepatic oxidative stress and inflammation are associated with elevated oxidative metabolism during an obesogenic diet, and this link may be provoked by increased work through anabolic pathways.