Enhanced-view totally extraperitoneal (eTEP) approach for the treatment of abdominal wall hernias: mid-term results.

INTRODUCTION: Multiple minimally invasive techniques have been described for ventral hernia repair. The recently described enhanced view totally extraperitoneal (eTEP) ventral hernia repair seems an appealing option since it allows to address midline and lateral hernias, placing the mesh in the retromuscular position without the use of traumatic fixation. AIM: To report on the mid-term result of a series of patients with ventral hernias repaired by the eTEP approach. METHODS: A retrospective analysis of our case series between June 2017 and December 2019. Demographic and clinical data were gathered. Hernia characteristics, surgical details, hernia recurrences, and complications are reported. RESULTS: 66 patients were included in the study. Median follow-up was 22 months (interquartile range 12-26). 60% of patients were male. Mean age, BMI, % of Type-2 diabetes and % of smoking were 59 ± 12 years, 30 kg/m2, 24% and 23%, respectively. Mean hernia defect size was 5.5 ± 2.9 cm. Forty-three eTEP Rives-stoppa and 23 eTEP-Transversus abdominis release (14 unilateral, 9 bilateral) were performed. 22 inguinal hernias and 15 lateral defects were simultaneously repaired. We report 1 recurrence (1.5%) and 10 surgical site occurrences (15%; 6 seromas, 2 hematomas and 2 surgical site infections). Four patients required reinterventions (6%). CONCLUSION: eTEP is a promising approach to treat midline hernias and allows the simultaneous treatment of lateral and inguinal defects, keeping the mesh in the retromuscular position. However, comparative studies must be performed to know its real benefit in laparoscopic ventral hernia repair.

Midterm Results of the Open and Minimally Invasive Transversus Abdominis Release Technique for the Treatment of Abdominal Wall Hernias in an Academic Center.

Introduction: Large hernia defects are a challenge for general and specialized hernia surgeons. The transversus abdominis release (TAR) technique has revolutionized the treatment of complex hernias since it allows the closure of large midline hernias, as well as hernias in different locations. This study aims to report the experience with the TAR technique and mid-term results in the first 101 patients. Methods: Non-concurrent cohort review of our prospectively collected electronic database. All patients submitted to a TAR (open or minimally invasive eTEP-TAR) from 2017 to 2020 were included. Demographic data, comorbidities, hernia characteristics, preoperative optimization, intraoperative variables, and clinical outcomes were gathered. The main outcomes of this study are hernia recurrences and surgical morbidity. Results: A total of 101 patients were identified. The median follow-up was 26 months. Mean age and body mass index was 63 years and 31.4 Kg/m2, respectively. Diabetes was present in 22% of patients and 43% had at least one previous hernia repair. Nineteen patients had significant loss of domain. Mean hernia size and area were 13 cm and 247 cm2, respectively. Ninety-six percent of cases were clean or clean-contaminated. The mean operative time was 164 min and all patients received a synthetic mesh. We diagnosed two hernia recurrences and the overall (medical and surgical) complication rate was 32%. The hernia-specific complication rate was 17%, with seven surgical site infections and seven surgical site occurrences requiring procedural interventions. Notably, weight loss was associated with a lower risk of SSOPI and reoperations. Conclusion: We show an encouraging 2% of recurrences in the mid-term follow-up in the setting of clinically complex hernia repair. However, we observed a high frequency of overall and hernia-specific complications pointing to the complexity of the type of surgery itself and the patients we operated on.

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure.

Acute renal failure (ARF) can be caused by injuries that induce tissue hypoxia, which in turn can trigger adaptive or inflammatory responses. We previously showed the participation of basic fibroblast growth factor (FGF-2) in renal repair. Based on this, the aim of this study was to analyze the effect of FGF-2 signaling pathway manipulation at hypoxia-induced protein levels, as well as in key proteins from the vasoactive systems of the kidney. We injected rat kidneys with FGF-2 recombinant protein (r-FGF) or FGF-2 receptor antisense oligonucleotide (FGFR2-ASO) after bilateral ischemia, and evaluated the presence of iNOS, EPO and HO-1, in representation of hypoxia-induced proteins, as well as COX-2, renin, kallikrein, and B2KR, in representation of the vasoactive systems of the kidney. A reduction in iNOS, HO-1, EPO, renin, kallikrein, B2KR, and in renal damage was observed in animals treated with r-FGF. The opposite effect was found with FGF-2 receptor down-regulation. In contrast, COX-2 protein levels were higher in kidneys treated with r-FGF and lower in those that received FGFR2-ASO, as compared to saline treated kidneys. These results suggest that the protective role of FGF-2 in the pathogenesis of ARF induced by I/R is a complex process, through which a differential regulation of metabolic pathways takes place.

Cyclooxygenase-2 and hypoxia-regulated proteins are modulated by basic fibroblast growth factor in acute renal failure

Acute renal failure (ARF) can be caused by injuries that induce tissue hypoxia, which in turn can trigger adaptive or inflammatory responses. We previously showed the participation of basic fibroblast growth factor (FGF-2) in renal repair. Based on this, the aim of this study was to analyze the effect of FGF-2 signaling pathway manipulation at hypoxia-induced protein levels, as well as in key proteins from the vasoactive systems of the kidney. We injected rat kidneys with FGF-2 recombinant protein (r-FGF) or FGF-2 receptor antisense oligonucleotide (FGFR2-ASO) after bilateral ischemia, and evaluated the presence of iNOS, EPO and HO-1, in representation of hypoxia-induced proteins, as well as COX-2, renin, kallikrein, and B2KR, in representation of the vasoactive systems of the kidney. A reduction in iNOS, HO-1, EPO, renin, kallikrein, B2KR, and in renal damage was observed in animals treated with r-FGF. The opposite effect was found with FGF-2 receptor down-regulation. In contrast, COX-2 protein levels were higher in kidneys treated with r-FGF and lower in those that received FGFR2-ASO, as compared to saline treated kidneys. These results suggest that the protective role of FGF-2 in the pathogenesis of ARF induced by I/R is a complex process, through which a differential regulation of metabolic pathways takes place.