Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.

Objective:To investigate the effect of galectin-3 (gal-3) on microglia polarization after subarachnoid hemorrhage (SAH).Methods:C57BL/6 male adult mice were used to induce SAH or sham operation models. Gal-3 siRNA or negative control siRNA was injected into the lateral ventricle 48 h before the model was induced. After 24 h of model preparation, the SAH score, neurological function score, brain water content, and Evans blue exudate were measured. Western blot analysis was used to detect the expressions of M1 phenotypic markers (inducible nitric oxide synthase [iNOS], CD11b, tumor necrosis factor [TNF]-α) and M2 phenotype markers (CD206, YM1/2, arginase-1 [Arg1]).Results:After using Gal-3 siRNA to inhibit Gal-3, the neurological function score significantly increased, while the SAH score, brain water content, and Evans blue exudate significantly decreased ( P<0.001). Western blot analysis showed that the expressions of M1 phenotypic markers (iNOS, CD11b and TNF-α) in microglia were significantly decreased after Gal-3 inhibition, while the expressions of M2 phenotypic markers (CD206, YM1/2 and Arg1) were significantly increased ( P<0.001). Conclusion:Inhibition of Gal-3 expression can alleviate the early brain injury after SAH, and its mechanism may be associated with regulating the polarization of microglia from M1 to M2 phenotype.

Objective:To investigate the effect of Sirtuin 1 (SIRT1) on subarachnoid hemorrhage (SAH) and its possible mechanism.Methods:A mouse model of SAH was constructed by internal carotid artery puncture. The protein and mRNA expression levels of SIRT1 at 0, 3, 6, 12, 24, 48, and 72 h were detected by Western Blot and qRT-PCR. A Western Blot assay was used to examine SIRT1 and the expression levels of endoplasmic reticulum stress-related markers GRP78, p-PERK/PERK, p-eIF2α/eIF2α, and CHOP after administration of a SIRT1 inhibitor or SIRT1 si-RNA. At 24 h after SAH, subarachnoid hemorrhage volume, neurological function score, brain water content, and blood-brain barrier integrity were measured.Results:The highest expression of SIRT1 protein and mRNA was observed at 24 h compared with other time points, and the differences were statistically significant (all P < 0.001). Inhibition of SIRT1 expression leads to increased expression of endoplasmic reticulum stress-related proteins GRP78, p-PERK/PERK, p-eIF2α/eIF2α, and CHOP, exacerbating hemorrhage and brain water content, disrupting blood-brain barrier integrity, and significantly reducing neurological function scores. Conclusions:Inhibition of SIRT1 expression significantly increased the endoplasmic reticulum response to excitation and exacerbated early brain injury after SAH.

Currently, the total ureteral avulsion are mainly secondary to ureteroscopy, and it is rarely caused by uterine evacuation clinically. This paper reported a case of total ureter avulsion after uterine evacuation, treating by ileal replacement for ureter under general anesthesia, and the surgical outcome was good. Uterine evacuation is a routine, less risky procedure, but it also can lead to serious complications such as total ureteral avulsion or bladder rupture. For potential high-risk patients with uterine evacuation, preventive measures such as accurate localization under B-ultrasound guidance or pre-operative ureteral stents indwelling are useful to avoid the occurrence of such serious complications. If total ureteral avulsion occurs, ileal replacement for ureter is a viable and effective treatment.

Objective:To conduct a bibliometric analysis of scientific publications on aneurysmal subarachnoid hemorrhage (aSAH) worldwide from 2012 to 2022 and to investigate the current research status and hotspots in this field.Methods:The Web of Science Core Collection was used as the data source. According to the set retrieval strategy, the CiteSpace bibliometric tools were used to analyze the published literature and explore the research hotspots and cutting-edge directions.Results:A total of 4 937 articles were included, and the number of publications increased year by year from 2012 to 2022. The United States is a leading country in this field, Harvard University is a leading institution in this field, and Rinkel Gabriel JE is the researcher with the most published articles in this field. The analysis of the keywords provided by the author showed that delayed cerebral ischemia, vasospasm, risk, intracranial aneurysms, endovascular treatment, risk factors, embolization, complications, Pipeline embolization device, coil embolization, hemodynamics, and wall shear stress were the main hotspots and cutting-edge directions of aSAH research.Conclusion:The results of bibliometric analysis help to grasp the current research status of aSAH and determine new directions for future research.

A recurrent misdiagnosed case of congenital left renal arteriovenous fistula (RAVF) with multiple left renal arteries and scoliosis was reported. The patient was admitted to hospital on 29 August 2020 due to repeated hematuria for one year. No abnormality was found in two flexible ureteroscope examinations, imaging and laboratory examinations after admission. It was found that the structure of blood vessels in the inferior pole of renal sinus was disordered, and the blood vessels were tortuous and clustered through careful reading of CT enhancement films. The dilated tortuous blood vessels were also seen around the renal pelvis, and hematuria was considered to be caused by renal vascular malformation. In order to confirm the etiology, digital subtraction angiography (DSA) of renal artery was performed. DSA showed a congenital left renal RAVF with three renal arteries, and the arteriovenous fistula of renal arteries was embolized. For patients presenting with severe gross hematuria, if tumor, stone, tuberculosis, or coagulation abnormalities were excluded by conventional imaging and/or laboratory examination the possibility of congenital renal vascular malformation should be suspected, and DSA examination should be performed. Endovascular embolization is an effective treatment for congenital RAVF.

Solitary kidney, renal duplication and malrotation are rare congenital renal malformations in urology department, and probably contributed to some complications such as obstruction, hydronephrosis, infection, stones. In this case report, we firstly presented a male patient with rarely multiple renal malformations, including solitary kidney, renal duplication, misaligned malrotation of upper and lower moieties, and accompanied by complete staghorn stones and hydronephrosis, who was treated with open pyelolithotomy under general anesthesia. After the operation, obstruction, hydronephrosis, and infection were relieved.

Objective:To investigate the effects of naringin on early brain injury in rats with subarachnoid hemorrhage and its possible mechanism of action.Methods:Rats were randomly divided into the sham operation group, the model group, and the naringin group. Each group had 8 rats. The SAH model was established by intravascular perforation, and then rats in the model group and the naringin group were administered 0.9% NaCl or naringin 40 mg/kg by intraperitoneal injection after 0.5 h. SAH score, neurological function score, cerebral edema, and blood-brain barrier permeability were detected. The level of NAD + and nflammatory factors were detected by ELISA. The expression of poly(ADP-ribose) polymerase-1 (PARP-1), apoptosis inducing factor (AIF), and protease-activated receptor (PAR) proteins was detected by Western Blot. The expression of PARP-1 mRNA was detected by quantitative real-time fluorescence PCR (qRT-PCR). Neuronal apoptosis was detected by an immunofluorescence assay. Results:Compared with the model group, naringin treatment improved neurological function ( P<0.01), reduced cerebral edema and Evans blue exudation (all P<0.01), increased the content of NAD + ( P<0.001), reduced IL-1β, IL-6 and TNF-α levels (all P<0.001), and reduced the expression of PARP-1/AIF pathway-related proteins in vivo (all P<0.001). In addition, naringin could inhibit neuronal apoptosis in early brain injury after SAH. Conclusions:Naringin can improve the early brain injury after SAH, which may be achieved by inhibiting the PARP-1/AIF pathway.

Objective:To explorethe the clinical manifestations, treatment and prognosis of anastomotic pseudoaneurysm after renal transplantation caused by infection.Methods:Clinical data of 1 recipient with pseudoaneurysm after renal transplantation due to Pseudomonas aeruginosa infection were retrospectively analysed and combined with a literature review. Results:At Month 2 post-transplantation, the recipient developed right lower abdominal pain, and contrast-enhanced ultrasound examination showed a pseudoaneurysm at the artery anastomosis. Anti-infection and anti-rejection therapy had no obvious effect, and therefore next surgical exploration was performed. A size4.0 cm×3.5cm pseudoaneurysm was found intraoperatively at the graft renal artery anastomosis.After graft was evaluated as having no preservation value, the transplanted kidney and pseudoaneurysm were resected. Bacterial culture indicated Pseudomonas aeruginosa infection.The recipient recovered well and waited for next transplantation. Conclusions:Pseudoaneurysm of transplanted kidney is a very rare complication after renal transplantation, and caused by infection of Pseudomonas aeruginosa is more rarer, It has not been reported in mainland China.This type of recipient has the characteristics of high graft inactivation rate and high mortality rate. Timely surgical resection can effectively prevent the deterioration of disease.

Objective:To investigate the effect of rutin on blood-brain barrier in early brain injury after subarachnoid hemorrhage (SAH) in rats.Methods:A rat model of SAH was induced by puncturing the internal carotid artery. The rats were divided into a sham operation group, a model group and a rutin (50 mg/kg) group. Twenty-four hours after modeling, SAH score and neurological deficit score were conducted, and brain water content and Evans blue extravasation rate were detected in each group. Western blot analysis was used to detect the expression of claudin-5, occludin and zonula occluden (ZO)-1. TUNEL staining was used to detect neuronal apoptosis.Results:Compared with the sham operation group, the SAH score increased, the neurological deficit score decreased, and the brain water content and Evans blue extravasation increased in the model group. Rutin could significantly reduce the SAH score, increase neurological deficit score, and reduce brain water content and Evans blue exudation (all P<0.01). Western blot analysis showed that the expression of claudin-5, occludin and ZO-1 protein decreased in the model group, and the expression of claudin-5, occludin and ZO-1 protein increased significantly in the rutin group ( P<0.01). In addition, the number of TUNEL positive cells induced by SAH in the rutin group decreased. Conclusion:Rutin can play a protective role in early brain injury after SAH, and its mechanism may be associated with protecting the integrity of blood-brain barrier.