Background Wound infection after inguinal hernia surgery is not uncommon in the clinical setting. The common microbial aetiology of postoperative inguinal hernia wound infection is Gram-positive bacteria. Staphylococcus aureus is a common pathogen causing wound infection while Staphylococcus epidermidis and Pseudomonas are rare. Staphylococcus epidermidis as a cause of severe wound infection is rarely described in literature. We herein present a case of a 79-year-old man with a rare wound infection after bilateral inguinal herniorrhaphy caused by MRCNS (Methicillin Resistant Coagulase Negative Staphylococcus ). Case presentation We present a case of wound infection accompanied by fever with a temperature of 38.8 °C after bilateral inguinal herniorrhaphy in a 79-year-old man. Bilateral inguinal wounds were marked by redness and swelling, with skin necrosis. In addition, an abscess of approximately 1.5 cm × 1.5 cm was seen on the left wrist. A small amount of gas under the skin in the wound area was observed after pelvic computed tomography (CT) scans. No bacteria were cultured from the inguinal wound discharge, while blood culture detected MRCNS, and Acinetobacter lwoffi was cultured from the pus in the left wrist. We chose appropriate antibiotics based on the results of the bacterial culture and the drug susceptibility results. Vacuum assisted closure (VAC) therapy was used after debridement. The patient was discharged after the wounds improved. He was followed up for ten months and showed no signs of complications. We are sharing our experience along with literature review. Conclusions We are presenting a rare case of MRCNS wound infection following open inguinal hernia surgery. Although a rarity, clinicians performing inguinal hernia surgery must consider this entity in an infected wound and follow up the patient for complications of MRCNS.

Background. Apoptosis plays an important role in various diseases, including spinal cord injury (SCI). Hyperbaric oxygen (HBO) and erythropoietin (EPO) promote the recovery from SCI, but the relationship between apoptosis and the combination therapeutic effect is not completely clear. Objective. The purpose of this study was to investigate the effects of HBO and EPO on SCI and the mechanisms that underlie their therapeutic benefits. Design. The study was designed to explore the effects of HBO and EPO on SCI through a randomized controlled trial. Methods. Sixty young developing female Sprague-Dawley rats were randomly divided into groups of 12 rats receiving sham, SCI, HBO, EPO, or HBO plus EPO. The SCI model was modified with the Allen method to better control consistency. HBO was performed for 1 hour per day for a total of 21 days, and EPO was given once per week for a total of 3 weeks. Both methods were performed 2 hours after SCI. Locomotor function was evaluated with the 21-point Basso-Beattie-Bresnahan Locomotor Rating Scale, an inclined-plane test, and a footprint analysis. All genes were detected by Western blotting and immunohistochemistry. The level of cell apoptosis was determined by Hoechst staining. Results. The results showed that HBO and EPO promoted the recovery of locomotor function in the hind limbs of rats by inhibiting the apoptosis of neurons. During this period, the expression of B-cell lymphoma/leukemia 2 protein (Bcl-2) increased significantly, whereas the expression of Bcl-2-associated X protein (Bax) and cleaved caspase 3 decreased significantly, indicating the inhibition of apoptosis. Meanwhile, the expression of G protein-coupled receptor 17 decreased, and that of myelin basic protein increased, suggesting that there may be a potential connection between demyelination and neuronal apoptosis. Limitations. The limitations of the study include deviations in the preparation of SCI models; lack of reverse validation of molecular mechanisms; absence of in vitro cell experiments; and only one time point after SCI was studied. Conclusions. HBO and EPO treatments are beneficial for SCI, especially when the 2 therapies are combined.

Background Inflammation and glial scar formation determine the recovery process after spinal cord injury. Hyperbaric oxygen is used as a rehabilitation therapy for various clinical diseases, including spinal cord injury. However, the relationship between hyperbaric oxygen therapy and inflammation or glial scar is not fully understood. Objective The aim of this study was to investigate the therapeutic effect and molecular mechanism of hyperbaric oxygen on spinal cord injury. Methods A total of 54 developing female Sprague-Dawley rats were randomly divided into sham group, spinal cord injury group, and hyperbaric oxygen group, with 18 rats in each group. The model of spinal cord injury was established using Allen's method. Hyperbaric oxygen therapy was administered once a day until the rats were killed. Results The results demonstrated inflammation and glial scar formation are involved in secondary spinal cord injury. After hyperbaric oxygen treatment, there was a notable improvement of the locomotor function in rats. Hyperbaric oxygen reduced the inflammatory reaction and glial scar formation by inhibiting inflammation-related factors iNOS and COX-2 and glial scar-related components GFAP and NG2. This process may be achieved by inhibiting AKT and NF-kB pathways. Conclusions Hyperbaric oxygen effectively promotes the recovery of spinal cord injury by inhibiting inflammation and glial scar formation.