Female sex and ipsilateral reoperation risk following mesh-based inguinal hernia repair: a cohort study including 131,626 repairs in adults from an integrated healthcare system over a 10-year period.

PURPOSE: We sought to compare females and males for the risk of reoperation following different inguinal hernia repair approaches (open, laparoscopic, and robotic). METHODS: We conducted a retrospective cohort study including all patients aged ≥ 18 who underwent first inguinal hernia repair with mesh within a US integrated healthcare system (2010-2020). Data were obtained from the system's integrated electronic health record. Multiple Cox proportional-hazards regression was used to evaluate the association between sex and risk for ipsilateral reoperation during follow-up. Analysis was stratified by surgical approach (open, laparoscopic, and robotic). RESULTS: The study cohort was comprised of 110,805 patients who underwent 131,626 inguinal hernia repairs with mesh, 10,079 (7.7%) repairs were in females. After adjustment for confounders, females had a higher risk of reoperation than males following open groin hernia repair (hazard ratio [HR] = 1.98, 95% CI 1.74-2.25), but a lower reoperation risk following laparoscopic repair (HR = 0.70, 95% CI 0.51-0.97). The crude 5-year cumulative reoperation probability following robotic repair was 2.8% in males and no reoperations were observed for females. Of females who had a reoperation, 10.3% (39/378) were for a femoral hernia, while only 0.6% (18/3110) were for femoral hernias in males. CONCLUSION: In a large multi-center cohort of mesh-based inguinal hernia repair patients, we found a higher risk for reoperation in females after an open repair approach compared to males. Lower risk was observed for females through a minimally invasive approach (laparoscopic or robotic) and may be due to the ability to identify an occult femoral hernia through these approaches.

Risk factors for reoperation following inguinal hernia repair: results from a cohort of patients from an integrated healthcare system.

PURPOSE: Inguinal hernia repair is one of the most common operations performed globally. Identification of risk factors that contribute to hernia recurrence following an index inguinal hernia repair, especially those that are modifiable, is of paramount importance. Therefore, we sought to investigate risk factors for reoperation following index inguinal hernia repair. METHODS: 125,133 patients aged ≥ 18 years who underwent their first inguinal hernia repair with mesh within a large US integrated healthcare system were identified for a cohort study (2010-2020). Laparoscopic, robotic, and open procedures were included. The system's integrated electronic health record was used to obtain data on demographics, patient characteristics, surgical characteristics, and reoperations. The association of these characteristics with ipsilateral reoperation during follow-up was modeled using Cox proportional-hazards regression. Risk factors were selected into the final model by stepwise regression with Akaike Information Criteria, which quantifies the amount of information lost if a factor is left out of the model. Factors associated with reoperation with p < 0.05 were considered statistically significant. RESULTS: The cumulative incidence of reoperation at 5-year follow-up was 2.4% (95% CI 2.3-2.5). Increasing age, female gender, increasing body mass index, White race, chronic pulmonary disease, diabetes, drug abuse, peripheral vascular disease, and bilateral procedures all associated with a higher risk for reoperation during follow-up. CONCLUSION: This study identifies several risk factors associated with reoperation following inguinal hernia repair. These risk factors may serve as targets for optimization protocols prior to elective inguinal hernia repair, with the goal of reducing reoperation risk.

Mesh-based inguinal hernia repairs in an integrated healthcare system and surgeon and hospital volume: a cohort study of 110,808 patients from over a decade.

PURPOSE: The aim of this study was to describe a cohort of patients who underwent inguinal hernia repair within a United States-based integrated healthcare system (IHS) and evaluate the risk for postoperative events by surgeon and hospital volume within each surgical approach, open, laparoscopic, and robotic. METHODS: Patients aged ≥ 18 years who underwent their first inguinal hernia repair were identified for a cohort study (2010-2020). Average annual surgeon and hospital volume were broken into quartiles with the lowest volume quartile as the reference group. Multiple Cox regression evaluated risk for ipsilateral reoperation following repair by volume. All analyses were stratified by surgical approach (open, laparoscopic, and robotic). RESULTS: 110,808 patients underwent 131,629 inguinal hernia repairs during the study years; procedures were performed by 897 surgeons at 36 hospitals. Most repairs were open (65.4%), followed by laparoscopic (33.5%) and robotic (1.1%). Reoperation rates at 5 and 10 years of follow-up were 2.4% and 3.4%, respectively; rates were similar across surgical groups. In adjusted analysis, surgeons with higher laparoscopic volumes had a lower reoperation risk (27-46 average annual repairs: hazard ratio [HR] = 0.63, 95% confidence interval [CI] 0.53-0.74; ≥ 47 repairs: HR 0.53, 95% CI 0.44-0.64) compared to those in the lowest volume quartile (< 14 average annual repairs). No differences in reoperation rates were observed in reference to surgeon or hospital volume following open or robotic inguinal hernia repair. CONCLUSION: High-volume surgeons may reduce reoperation risk following laparoscopic inguinal hernia repair. We hope to better identify additional risk factors for inguinal hernia repair complications and improve patient outcomes with future studies.

MK-801 inhibits the induction of immediate early genes in cerebral cortex, thalamus, and hippocampus, but not in substantia nigra following middle cerebral artery occlusion.

Middle cerebral artery (MCA) occlusion in rats induced c-fos and junB mRNA 4h later in all ipsilateral cortex outside the MCA distribution and in many subcortical structures: medial striatum; most of thalamus including medial and lateral geniculate nuclei: substantia nigra; and hippocampus. The N-methyl-D-aspartate (NMDA) antagonist, MK-801 (4 mg/kg, i.p.) inhibited c-fos and junB mRNA induction in the cortex, striatum, thalamus, and hippocampus but not in the substantia nigra. These data show that c-fos and junB mRNA induction in cortex, striatum, thalamus, hippocampus involves the activation of NMDA receptors whereas different receptors must be implicated in the induction in substantia nigra.

Lipid peroxidation does not appear to be a factor in late radiation injury of the cervical spinal cord of rats.

PURPOSE: We tested the role of lipid peroxidation in the demyelination and white matter necrosis associated with radiation injury of the central nervous system. METHODS AND MATERIALS: We irradiated the cervical spinal cords of female F344 rats (23 Gy) and assayed for the accumulation of the peroxidation byproducts malondialdehyde and hydroxyeicosatetraenoic acids, and for the consumption of the endogenous free radical scavengers vitamins E and C. We further tested the role of lipid peroxidation in radiation injury of the central nervous system by determining the sensitivity of the cervical spinal cord to radiation in rats on diets containing deficient, normal, and supplemental levels of the antioxidant vitamin E. Rats were placed on these diets at 4 weeks of age and irradiated (18.5-21.5 Gy) 16 weeks later. RESULTS: During the 5 months between irradiation and the onset of paralysis, no accumulation of peroxidation byproducts or consumption of endogenous scavengers was seen in the cervical spinal cords of the irradiated rats. The cervical spinal cords of some of the rats placed on the diets with deficient, normal, and supplemental levels of vitamin E were analyzed at the time of irradiation and contained 197 +/- 57, 501 +/- 19, and 717 +/- 35 pmol vitamin E/mg protein, respectively. Despite the statistical differences in these levels, the radiation sensitivity of the cervical spinal cord (ED50 for white matter necrosis) in rats receiving the three diets was not different (20.4, 20.7, and 20.6 Gy). CONCLUSION: These data do not support a role for free radical-induced lipid peroxidation in the white matter damage seen in radiation injury of the central nervous system.

Glutamine stimulates growth in rat cerebral endothelial cell culture.

Endothelial cells were isolated from rat cerebral cortices using combined enzymatic digestions and Percoll gradient centrifugation. Primary cultures were subsequently grown on collagen-covered dishes in a medium containing 20% fetal calf serum and 0.6 mmol glutamine. The majority of cultures became confluent by day 7 or 8, but some could not reach confluence. The cells were fusiform in shape and exhibited immunoreactivity to factor VIII-related antigen and binding to the lectin Griffonia simplicifolia. Exposure of cultures to media containing 2.6 mmol glutamine resulted in accelerated growth (in cultures were confluent at days 3-4) and change in culture morphology, namely the formation of circular, cell-free areas. However, this treatment did not restore gamma-glutamyl transpeptidase activity that was lost during cultivation. As for other amino acids, asparagine was less potent, glycine and phenylalanine failed to mimic the glutamine effect. In summary, glutamine stimulates growth of cerebral endothelial cells in vitro and so it may supplement for other growth factors in the culture media.