Bilateral vertebral artery injury leads to brain death following traumatic brain injury: a case report.

BACKGROUND: Vertebral artery injury is a rare condition in trauma settings. In the advanced stages, it causes death. CASE: A 31-year-old Sundanese woman with cerebral edema, C2-C3 anterolisthesis, and Le Fort III fracture after a motorcycle accident was admitted to the emergency room. On the fifth day, she underwent arch bar maxillomandibular application and debridement in general anesthesia with a hyperextended neck position. Unfortunately, her rigid neck collar was removed in the high care unit before surgery. Her condition deteriorated 72 hours after surgery. Digital subtraction angiography revealed a grade 5 bilateral vertebral artery injury due to cervical spine displacement and a grade 4 left internal carotid artery injury with a carotid cavernous fistula (CCF). The patient was declared brain death as not improved cerebral perfusion after CCF coiling. CONCLUSIONS: Brain death due to cerebral hypoperfusion following cerebrovascular injury in this patient could be prevented by early endovascular intervention and cervical immobilisation.

Coptisine inhibits neointimal hyperplasia through attenuating Pak1/Pak2 signaling in vascular smooth muscle cells without retardation of re-endothelialization.

BACKGROUND AND AIMS: Vascular injury-induced endothelium-denudation and profound vascular smooth muscle cells (VSMCs) proliferation and dis-regulated apoptosis lead to post-angioplasty restenosis. Coptisine (CTS), an isoquinoline alkaloid, has multiple beneficial effects on the cardiovascular system. Recent studies identified it selectively inhibits VSMCs proliferation. However, its effects on neointimal hyperplasia, re-endothelialization, and the underlying mechanisms are still unclear. METHODS: Cell viability was assayed by 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and cell counting kit-8 (CCK-8). Cell proliferation and apoptosis were measured by flow cytometry and immunofluorescence of Ki67 and TUNEL. Quantitative phosphoproteomics (QPP) was employed to screen CTS-responsive phosphor-sites in the key regulators of cell proliferation and apoptosis. Neointimal hyperplasia was induced by balloon injury of rat left carotid artery (LCA). Adenoviral gene transfer was conducted in both cultured cells and LCA. Re-endothelialization was evaluated by Evan's blue staining of LCA. RESULTS: 1) CTS had strong anti-proliferative and pro-apoptotic effects in cultured rat VSMCs, with the EC50 4∼10-folds lower than that in endothelial cells (ECs). 2) Rats administered with CTS, either locally to LCA's periadventitial space or orally, demonstrated a potently inhibited balloon injury-induced neointimal hyperplasia, but had no delaying effect on re-endothelialization. 3) The QPP results revealed that the phosphorylation levels of Pak1S144/S203, Pak2S20/S197, Erk1T202/Y204, Erk2T185/Y187, and BadS136 were significantly decreased in VSMCs by CTS. 4) Adenoviral expression of phosphomimetic mutants Pak1D144/D203/Pak2D20/D197 enhanced Pak1/2 activities, stimulated the downstream pErk1T202/Y204/pErk2T185/Y187/pErk3S189/pBadS136, attenuated CTS-mediated inhibition of VSMCs proliferation and promotion of apoptosis in vitro, and potentiated neointimal hyperplasia in vivo. 5) Adenoviral expression of phosphoresistant mutants Pak1A144/A203/Pak2A20/A197 inactivated Pak1/2 and totally simulated the inhibitory effects of CTS on platelet-derived growth factor (PDGF)-stimulated VSMCs proliferation and PDGF-inhibited apoptosis in vitro and neointimal hyperplasia in vivo. 6) LCA injury significantly enhanced the endogenous phosphorylation levels of all but pBadS136. CTS markedly attenuated all the enhanced levels. CONCLUSIONS: These results indicate that CTS is a promising medicine for prevention of post-angioplasty restenosis without adverse impact on re-endothelialization. CTS-directed suppression of pPak1S144/S203/pPak2S20/S197 and the subsequent effects on downstream pErk1T202/Y204/pErk2T185/Y187/pErk3S189 and pBadS136 underline its mechanisms of inhibition of VSMCs proliferation and stimulation of apoptosis. Therefore, the phosphor-sites of Pak1S144/S203/Pak2S20/S197 constitute a potential drug-screening target for fighting neointimal hyperplasia restenosis.

Exosomes of endothelial progenitor cells repair injured vascular endothelial cells through the Bcl2/Bax/Caspase-3 pathway.

The main objective of this study is to evaluate the influence of exosomes derived from endothelial progenitor cells (EPC-Exo) on neointimal formation induced by balloon injury in rats. Furthermore, the study aims to investigate the potential of EPC-Exo to promote proliferation, migration, and anti-apoptotic effects of vascular endothelial cells (VECs) in vitro. The underlying mechanisms responsible for these observed effects will also be thoroughly explored and analyzed. Endothelial progenitor cells (EPCs) was isolated aseptically from Sprague-Dawley (SD) rats and cultured in complete medium. The cells were then identified using immunofluorescence and flow cytometry. The EPC-Exo were isolated and confirmed the identities by western-blot, transmission electron microscope, and nanoparticle analysis. The effects of EPC-Exo on the rat carotid artery balloon injury (BI) were detected by hematoxylin and eosin (H&E) staining, ELISA, immunohistochemistry, immunofluorescence, western-blot and qPCR. LPS was used to establish an oxidative damage model of VECs. The mechanism of EPC-Exo repairing injured vascular endothelial cells was detected by measuring the proliferation, migration, and tube function of VECs, actin cytoskeleton staining, TUNEL staining, immunofluorescence, western-blot and qPCR. In vivo, EPC-Exo exhibit inhibitory effects on neointima formation following carotid artery injury and reduce the levels of inflammatory factors, including TNF-α and IL-6. Additionally, EPC-Exo downregulate the expression of adhesion molecules on the injured vascular wall. Notably, EPC-Exo can adhere to the injured vascular area, promoting enhanced endothelial function and inhibiting vascular endothelial hyperplasia Moreover, they regulate the expression of proteins and genes associated with apoptosis, including B-cell lymphoma-2 (Bcl2), Bcl2-associated x (Bax), and Caspase-3. In vitro, experiments further confirmed that EPC-Exo treatment significantly enhances the proliferation, migration, and tube formation of VECs. Furthermore, EPC-Exo effectively attenuate lipopolysaccharides (LPS)-induced apoptosis of VECs and regulate the Bcl2/Bax/Caspase-3 signaling pathway. This study demonstrates that exosomes derived from EPCs have the ability to inhibit excessive carotid intimal hyperplasia after BI, promote the repair of endothelial cells in the area of intimal injury, and enhance endothelial function. The underlying mechanism involves the suppression of inflammation and anti-apoptotic effects. The fundamental mechanism for this anti-apoptotic effect involves the regulation of the Bcl2/Bax/Caspase-3 signaling pathway.

Endovascular Treatment of Traumatic Vascular Injuries in the Head and Neck Region.

Background and Objectives: Traumatic vascular injuries of the head and neck pose significant treatment challenges due to the complex anatomy, diverse clinical presentation, and mostly emergent nature. Endovascular treatment increasingly complements traditional surgical approaches. This study aimed to report our 10-year experience in treating traumatic vascular injuries of the head and neck with endovascular therapy and to determine the effectiveness of endovascular treatment. Materials and Methods: A retrospective analysis of 21 patients treated for head and neck vascular injuries between May 2011 and April 2021 was performed. Patients' medical histories, clinical presentations, imaging findings, treatment materials, and clinical outcomes were reviewed. Treatments included stenting, coil embolization, and other endovascular techniques focused on hemostasis and preservation of the parent vessel. Results: The most common injuries involved the internal maxillary artery branches (n = 11), followed by the common or internal carotid artery (n = 6), vertebral artery (n = 3), and others. Endovascular treatment achieved successful hemostasis in all but one case. In five of six carotid artery injuries and two of three vertebral artery injuries, we achieved successful hemostasis while preserving the parent vessel using covered and bare stents, respectively. Conclusions: Endovascular therapy might be a useful treatment modality for traumatic vascular injuries in the head and neck region, offering efficacy, safety, and a minimally invasive approach.

Stenting for Traumatic Pseudoaneurysms of the Cervical Internal Carotid Artery: Case Report and Systematic Review.

BACKGROUND: The optimal stenting approach for traumatic pseudoaneurysms (PSA) of the extracranial internal carotid artery (ICA) remains underinvestigated. We present a case of a traumatic pseudoaneurysm of the extracranial ICA managed with stenting and review of prior published similar cases. METHODS: The systematic review followed PRISMA-S guidelines and included studies that investigated traumatic pseudoaneurysms of the extracranial ICA managed by stent placement. Statistical analysis assessed the association between the type of injury and stent type, dual antiplatelet therapy (DAPT) duration, and clinical presentation, and the association between stent type and DAPT duration. RESULTS: Our search yielded 82 publications with 135 patients with extracranial ICA PSA treated with stenting. The odds of neck hematoma presentation was 12.2 times greater for patients with penetrating rather than blunt injuries (P = 0.000002). Covered stents had 2.02 times higher odds of use for penetrating rather than blunt injuries compared to bare metal stents. (P = 0.0029). Shorter duration DAPT was seen with bare metal stents having 1.25 higher odds of DAPT duration less than one month compared to covered (P = 0.001). CONCLUSIONS: In traumatic extracranial ICA pseudoaneurysms, covered stents are used more commonly for penetrating injuries compared to blunt injuries. Penetrating injuries are more strongly associated with the presentation of a hematoma compared to blunt injuries. Stent type may influence the recommended DAPT duration. Surgeons should consider these findings when selecting stent type and DAPT duration with patients presenting with traumatic extracranial ICA pseudoaneurysm.

Atlas of Cell Repertoire Within Neointimal Lesions Is Metabolically Altered in Hypertensive Rats.

BACKGROUND: High blood pressure has been suggested to accelerate vascular injury-induced neointimal formation and progression. However, little is known about the intricate relationships between vascular injury and hypertension in the context of arterial remodeling. METHODS: Single-cell RNA-sequencing analysis was used to depict the cell atlas of carotid arteries of Wistar Kyoto rats and spontaneously hypertensive rats with or without balloon injury. RESULTS: We found that hypertension significantly aggravated balloon injury-induced arterial stenosis. A total of 36 202 cells from carotid arteries with or without balloon injury were included in single-cell RNA-sequencing analysis. Cell composition analysis showed that vascular injury and hypertension independently induced distinct aortic cell phenotypic alterations including immune cells, endothelial cells (ECs), and smooth muscle cells. Specifically, our data showed that injury and hypertension-induced specific EC phenotypic alterations, and revealed a transition from functional ECs to hypermetabolic, and eventually dysfunctional ECs in hypertensive rats upon balloon injury. Importantly, our data also showed that vascular injury and hypertension-induced different smooth muscle cell phenotypic alterations, characterized by deferential expression of synthetic signatures. Interestingly, pathway analysis showed that dysregulated metabolic pathways were a common feature in monocytes/macrophages, ECs, and smooth muscle cells in response to injury and hypertension. Functionally, we demonstrate that inhibition of mitochondrial respiration significantly ameliorated injury-induced neointimal formation in spontaneously hypertensive rats. CONCLUSIONS: This study provides the cell landscape changes of the main aortic cell phenotypic alterations in response to injury and hypertension. Our findings suggest that targeting cellular mitochondrial respiration could be a novel therapeutic for patients with hypertension undergoing vascular angioplasty.

Transfer RNA-derived small RNA tRF-Glu-CTC attenuates neointimal formation via inhibition of fibromodulin.

Neointimal hyperplasia is a pathological vascular remodeling caused by abnormal proliferation and migration of subintimal vascular smooth muscle cells (VSMCs) following intimal injury. There is increasing evidence that tRNA-derived small RNA (tsRNA) plays an important role in vascular remodeling. The purpose of this study is to search for tsRNAs signature of neointima formation and to explore their potential functions. The balloon injury model of rat common carotid artery was replicated to induce intimal hyperplasia, and the differentially expressed tsRNAs (DE-tsRNAs) in arteries with intimal hyperplasia were screened by small RNA sequencing and tsRNA library. A total of 24 DE-tsRNAs were found in the vessels with intimal hyperplasia by small RNA sequencing. In vitro, tRF-Glu-CTC inhibited the expression of fibromodulin (FMOD) in VSMCs, which is a negative modulator of TGF-ß1 activity. tRF-Glu-CTC also increased VSMC proliferation and migration. In vivo experiments showed that inhibition of tRF-Glu-CTC expression after balloon injury of rat carotid artery can reduce the neointimal area. In conclusion, tRF-Glu-CTC expression is increased after vascular injury and inhibits FMOD expression in VSMCs, which influences neointima formation. On the other hand, reducing the expression of tRF-Glu-CTC after vascular injury may be a potential approach to prevent vascular stenosis.

Potassium dehydroandrographolide succinate regulates the MyD88/CDH13 signaling pathway to enhance vascular injury-induced pathological vascular remodeling.

Pathological vascular remodeling is a hallmark of various vascular diseases. Previous research has established the significance of andrographolide in maintaining gastric vascular homeostasis and its pivotal role in modulating endothelial barrier dysfunction, which leads to pathological vascular remodeling. Potassium dehydroandrographolide succinate (PDA), a derivative of andrographolide, has been clinically utilized in the treatment of inflammatory diseases precipitated by viral infections. This study investigates the potential of PDA in regulating pathological vascular remodeling. The effect of PDA on vascular remodeling was assessed through the complete ligation of the carotid artery in C57BL/6 mice. Experimental approaches, including rat aortic primary smooth muscle cell culture, flow cytometry, bromodeoxyuridine (BrdU) incorporation assay, Boyden chamber cell migration assay, spheroid sprouting assay, and Matrigel-based tube formation assay, were employed to evaluate the influence of PDA on the proliferation and motility of smooth muscle cells (SMCs). Molecular docking simulations and co-immunoprecipitation assays were conducted to examine protein interactions. The results revealed that PDA exacerbates vascular injury-induced pathological remodeling, as evidenced by enhanced neointima formation. PDA treatment significantly increased the proliferation and migration of SMCs. Further mechanistic studies disclosed that PDA upregulated myeloid differentiation factor 88 (MyD88) expression in SMCs and interacted with T-cadherin (CDH13). This interaction augmented proliferation, migration, and extracellular matrix deposition, culminating in pathological vascular remodeling. Our findings underscore the critical role of PDA in the regulation of pathological vascular remodeling, mediated through the MyD88/CDH13 signaling pathway.

Prognostic factors associated with risk of stroke following blunt cerebrovascular injury: A systematic review and meta-analysis.

BACKGROUND & OBJECTIVES: Blunt cerebrovascular injury (BCVI) includes carotid and/or vertebral artery injury following trauma, and conveys an increased stroke risk. We conducted a systematic review and meta-analysis to provide a comprehensive summary of prognostic factors associated with risk of stroke following BCVI. METHODS: We searched the EMBASE and MEDLINE databases from January 1946 to June 2023. We identified studies reporting associations between patient or injury factors and risk of stroke following BCVI. We performed meta-analyses of odds ratios (ORs) using the random effects method and assessed individual study risk of bias using the QUIPS tool. We separately pooled adjusted and unadjusted analyses, highlighting the estimate with the higher certainty. RESULTS: We included 26 cohort studies, involving 20,458 patients with blunt trauma. The overall incidence of stroke following BCVI was 7.7 %. Studies were predominantly retrospective cohorts from North America and included both carotid and vertebral artery injuries. Diagnosis of BCVI was most commonly confirmed with CT angiography. We demonstrated with moderate to high certainty that factors associated with increased risk of stroke included carotid artery injury (as compared to vertebral artery injury, unadjusted odds ratio [uOR] 1.94, 95 % CI 1.62 to 2.32), Grade III Injury (as compared to grade I or II) (uOR 2.45, 95 % CI 1.88 to 3.20), Grade IV injury (uOR 3.09, 95 % CI 2.20 to 4.35), polyarterial injury (uOR 3.11 (95 % CI 2.05 to 4.72), occurrence of hypotension at the time of hospital admission (adjusted odds ratio [aOR] 1.32, 95 % CI 0.87 to 2.03) and higher total body injury severity (aOR 5.91, 95 % CI 1.90 to 18.39). CONCLUSION: Local anatomical injury pattern, overall burden of injury and flow dynamics contribute to BCVI-related stroke risk. These findings provide the foundational evidence base for risk stratification to support clinical decision making and further research.

Ultrasound-guided periadventitial administration of rapamycin-fibrin glue attenuates neointimal hyperplasia in the rat carotid artery injury model.

INTRODUCTION: Arterial restenosis caused by intimal hyperplasia (IH) is a serious complication after vascular interventions. In the rat carotid balloon injury model, we injected phosphate buffer saline (PBS), rapamycin-phosphate buffer saline suspension (RPM-PBS), blank fibrin glue (FG) and rapamycin-fibrin glue (RPM-FG) around the injured carotid artery under ultrasound guidance and observed the inhibitory effect on IH. METHODS: The properties of RPM-FG in vitro were verified by scanning electron microscopy (SEM) and determination of the drug release rate. FG metabolism in vivo was observed by fluorescence imaging. The rat carotid balloon injury models were randomly classified into 4 groups: PBS group (control group), RPM-PBS group, FG group, and RPM-FG group. Periadventitial administration was performed by ultrasound-guided percutaneous puncture on the first day after angioplasty. Carotid artery specimens were analyzed by immunostaining, Evans blue staining and hematoxylin-eosin staining. RESULTS: The RPM particles showed clustered distributions in the FG block. The glue was maintained for a longer time in vivo (> 14 days) than in vitro (approximately 7 days). Two-component liquid FG administered by ultrasound-guided injection completely encapsulated the injured artery before coagulation. The RPM-FG inhibited IH after carotid angioplasty vs. control and other groups. The proliferation of vascular smooth muscle cells (VSMCs) was significantly inhibited during neointima formation, whereas endothelial cell (EC) repair was not affected. CONCLUSION: Periadventitial delivery of RPM-FG contributed to inhibiting IH in the rat carotid artery injury model without compromising re-endothelialization. Additionally, FG provided a promising platform for the future development of a safe, effective, and minimally invasive perivascular drug delivery method to treat vascular disease.

Internal carotid artery injury during endoscopic transsphenoidal pituitary surgery: risk factors, management.

BACKGROUND: Transsphenoidal surgeons should try to avoid internal carotid artery (ICA) injury but also be prepared to manage it. We analyzed our experience with ICA injury during endoscopic transsphenoidal pituitary surgery and present associated risk factors and a management protocol. METHODS: We retrospectively reviewed and analyzed the medical records of 1596 patients who underwent endoscopic transsphenoidal surgery for pituitary tumor resection in our institution from January 2009 to October 2022. RESULTS: Six patients experienced an ICA injury. All received timely and effective hemostasis with immediate direct tamponade followed by endovascular treatment. No serious postoperative complications occurred. CONCLUSIONS: We proposed a treatment plan for ICA injuries encountered during endoscopic transsphenoidal surgery and described our hemostasis process, methods of endovascular treatment, and means of postoperative follow-up in detail.

Methyl donor diet attenuates intimal hyperplasia after vascular injury in rats.

Environmental factors, particularly dietary habits, play an important role in cardiovascular disease susceptibility and progression through epigenetic modification. Previous studies have shown that hyperplastic vascular intima after endarterectomy is characterized by genome-wide hypomethylation. The purpose of this study was to investigate whether methyl donor diet affects intimal hyperplasia and the possible mechanisms involved. Intimal hyperplasia was induced in SD rats by carotid artery balloon injury. From 8 d before surgery to 28 d after surgery, the animals were fed a normal diet (ND) or a methyl donor diet (MD) supplemented with folic acid, vitamin B12, choline, betaine, and zinc. Carotid artery intimal hyperplasia was observed by histology, the effect of MD on carotid protein expression was analyzed by proteomics, functional clustering, signaling pathway, and upstream-downstream relationship of differentially expressed proteins were analyzed by bioinformatics. Results showed that MD attenuated balloon injury-induced intimal hyperplasia in rat carotid arteries. Proteomic analysis showed that there were many differentially expressed proteins in the common carotid arteries of rats fed with two different diets. The differentially expressed proteins are mainly related to the composition and function of the extracellular matrix (EMC), and changes in the EMC can lead to vascular remodeling by affecting fibrosis and stiffness of the blood vessel wall. Changes in the levels of vasculotropic proteins such as S100A9, ILF3, Serpinh1, Fbln5, LOX, HSPG2, and Fmod may be the reason why MD attenuates intimal hyperplasia. Supplementation with methyl donor nutrients may be a beneficial measure to prevent pathological vascular remodeling after injury.

Analysis of Extracranial Cerebrovascular Injuries: Clinical Predictors of Management and Outcomes.

BACKGROUND: Optimal management of traumatic extracranial cerebrovascular injuries (ECVIs) remains undefined. We sought to evaluate the factors that influence management and neurologic outcomes (stroke and brain death) following traumatic ECVI. METHODS: A retrospective review of a single level 1 trauma center's prospectively maintained data registry of patients older than 18 years of age with a diagnosis of ECVI was performed from 2013 to 2019. Injuries limited to the external carotid artery were excluded. Patient demographics, type of injury, timing of presentation, Biffl Classification of Cerebrovascular Injury Grade, Injury Severity Score (ISS), and Abbreviated Injury Scale were documented. Ultimate treatments (medical management and procedural interventions) and brain-related outcomes (stroke and brain death) were recorded. RESULTS: ECVIs were identified in 96 patients. The primary mechanism of injury was blunt trauma (89.5% vs. 10.5%, blunt versus penetrating), with 70 cases (66%) of vertebral artery injury and 37 cases of carotid artery injury. Treatments included vascular intervention (6.5%) and medical management (93.5%). Overall outcomes included ipsilateral ischemic stroke (29%) and brain death (6.5%). In the carotid group, vascular intervention was associated with higher Biffl grades (mean Biffl 3.17 vs. 2.23; P = 0.087) and decreased incidence of brain death (0% vs. 19%, P = 0.006), with no difference seen in ISS scores. Brain death was associated with higher ISS scores (40.29 vs. 24.17, P = 0.01), lower glascow coma score on arrival (3.57 vs. 10.63, P < 0.001), and increased rates of ischemic stroke (71% vs. 30%, P = 0.025). In the vertebral group, neither Biffl grade nor ISS were associated with treatment or outcomes. Regarding the timing of stroke in ECVI, there was no significant difference in the time from presentation to cerebral infarction between the carotid and vertebral artery groups (24.7 hr vs. 21.20 hr, P = 0.739). After this window, 98% of the ECVI cases demonstrated no further aneurysmal degeneration or new neurological deficits beyond the early time period (mean follow-up 9.7 months). CONCLUSIONS: Blunt cerebrovascular injuries should be viewed distinctly in the carotid and vertebral territories. In cases of injury to the carotid artery, Biffl grade and ISS score are associated with surgical intervention and neurologic events, respectively; vertebral artery injuries did not share this association. Neurologic deficits were detected in a similar time frame between the carotid artery and the vertebral artery injury groups and both groups had rare late neurologic events.

Pilot Analysis of Surgeon Instrument Utilization Signatures Based on Shannon Entropy and Deep Learning for Surgeon Performance Assessment in a Cadaveric Carotid Artery Injury Control Simulation.

BACKGROUND AND OBJECTIVES: Assessment and feedback are critical to surgical education, but direct observational feedback by experts is rarely provided because of time constraints and is typically only qualitative. Automated, video-based, quantitative feedback on surgical performance could address this gap, improving surgical training. The authors aim to demonstrate the ability of Shannon entropy (ShEn), an information theory metric that quantifies series diversity, to predict surgical performance using instrument detections generated through deep learning. METHODS: Annotated images from a publicly available video data set of surgeons managing endoscopic endonasal carotid artery lacerations in a perfused cadaveric simulator were collected. A deep learning model was implemented to detect surgical instruments across video frames. ShEn score for the instrument sequence was calculated from each surgical trial. Logistic regression using ShEn was used to predict hemorrhage control success. RESULTS: ShEn scores and instrument usage patterns differed between successful and unsuccessful trials (ShEn: 0.452 vs 0.370, P < .001). Unsuccessful hemorrhage control trials displayed lower entropy and less varied instrument use patterns. By contrast, successful trials demonstrated higher entropy with more diverse instrument usage and consistent progression in instrument utilization. A logistic regression model using ShEn scores (78% accuracy and 97% average precision) was at least as accurate as surgeons' attending/resident status and years of experience for predicting trial success and had similar accuracy as expert human observers. CONCLUSION: ShEn score offers a summative signal about surgeon performance and predicted success at controlling carotid hemorrhage in a simulated cadaveric setting. Future efforts to generalize ShEn to additional surgical scenarios can further validate this metric.

Penetrating carotid artery injury by air rifle: a case report.

BACKGROUND: Air rifle injuries can cause significant vascular injuries. This air rifle injury has resulted in a penetrating neck trauma traversing the common carotid artery. There is debate around the need for radiological investigation, the most appropriate investigational modality, and the need for surgical exploration versus a conservative approach. This case report aims to exemplify a successful approach to managing Penetrating Carotid Injuries (PCI) while shedding light on the rationale behind the management decisions. PRESENTATION: An 18-year-old Caucasian man arrived at the hospital following an air rifle injury to the right side of the neck, with active bleeding and a moderate haematoma displacing the trachea. He was haemodynamically stable, with a Glasgow Coma Scale (GCS) of 15 and no evidence of bruit. Computed Tomography Angiography (CTA) showed Right common carotid (CCA) artery injury with associated post-traumatic pseudoaneurysm. The pellet trajectory traverses the right superior thyroid gland. A duplex ultrasound scan (USS) confirmed two areas of arterial blush at the right CCA. Management involved neck exploration under General Anaesthesia (G.A.), repair of right CCA, bullet extraction, and wound washout. He received antibiotics for ten days and a single agent of antiplatelets for three months and was discharged two days postoperatively with no complications. He was followed up for eight months with no evidence of any trauma sequelae. CONCLUSION: Penetrating carotid artery injuries are a serious concern. The small-sized pellets carry the risk of embolization. Therefore, neck exploration remains the gold standard treatment for PCI. Appropriate operative planning is crucial and can be optimised using radiological diagnostic modalities in haemodynamically stable patients. CTA is a non-invasive, swift, and adequate alternative to arteriography, providing valuable diagnostic information on vascular and aerodigestive injuries and bullet trajectory. This enables appropriate preparedness to achieve excellent outcomes in such critical cases.

Omentin-1 enhances the inhibitory effect of endothelial progenitor cells on neointimal hyperplasia by inhibiting the p38 MAPK/CREB pathway.

AIMS: Endothelial progenitor cells (EPCs) play an important role in vascular repair. However, they are dysfunctional in the inflammatory microenvironment during restenosis. In this study, we investigated whether omentin-1, an anti-inflammatory factor, could reduce neointima formation after carotid artery injury (CAI) in rats by improving EPC functions that were damaged by inflammation and the underlying mechanisms. MAIN METHODS: EPCs were transfected with adenoviral vectors expressing human omentin-1 or green fluorescent protein (GFP). Then, the rats received 2 × 106 EPCs expressing omentin-1 or GFP by tail vein injection directly after CAI and again 24 h later. Hematoxylin-eosin staining and immunohistochemistry were used for analyzing neointimal hyperplasia. Besides, EPCs were treated with omentin-1 and TNF-α to examine the underlying mechanism. KEY FINDINGS: Our results showed that omentin-1 could significantly improve EPC functions, including proliferation, apoptosis and tube formation. Meanwhile, EPCs overexpressed with omentin-1 could significantly reduce neointimal hyperplasia and tumor necrosis factor-α (TNF-α) expression after CAI in rats. TNF-α could notably induce EPC dysfunction, which could be markedly reversed by omentin-1 through the inhibition of the p38 MAPK/CREB pathway. Furthermore, a p38 MAPK agonist (anisomycin) significantly abrogated the protective effects of omentin-1 on EPCs damaged by TNF-α. SIGNIFICANCE: Our results indicated that genetically modifying EPC with omentin-1 could be an alternative strategy for the treatment of restenosis.

Exploring the role of endovascular interventions in blunt carotid and vertebral artery trauma.

BACKGROUND: The role of endovascular interventions (EI) for blunt carotid and vertebral artery injuries (BCI and BVI) is poorly defined. The purpose of this study was to assess the efficacy of EI compared with antithrombotic therapy (AT) to inform future prospective study. METHODS: Retrospective review (2017-2022) of records at a Level I trauma center to determine injury, treatment, and outcome information. Primary outcome was stroke. RESULTS: 96 patients suffered 106 injuries (74 BVI, 32 BCI). 12 patients underwent 13 EI- 4 therapeutic, 9 prophylactic. Stroke occurred in 12 patients- 6 who had EI. In grade IV BVI, stroke rates are low with both EI and AT. Thrombectomy after stroke improved neurologic function in 4 (100%) of 4 patients. CONCLUSIONS: Most strokes occur prior to preventive therapy. Neither AT nor EI is 100% effective in preventing stroke. Thrombectomy may improve neurologic outcomes after stroke. Prospective multicenter study is imperative.

Major Internal Carotid Artery Injury During Endoscopic Skull Base Surgery: Case Report.

Major vascular structures are always at risk during complex skull base surgery, particularly with use of the endoscopic endonasal approach, and intraoperative damage of the internal carotid artery (ICA) can be a devastating complication. Herein, we report a case of a young patient who had a major injury of the left ICA during endoscopic resection of a recurrent petrous bone chordoma. Massive bleeding was controlled by a Foley balloon inserted and kept in the resection area. Urgent angiography revealed a persistent leak from the petrous segment of the left ICA, and the vessel was sacrificed with coiling, since a balloon occlusion test showed good collateral blood flow. The patient woke up from anesthesia without a neurological deficit. Salvage resection of recurrent skull base neoplasms deserves specific attention because of the possibility of major vascular damage. In cases of intraoperative ICA injury, its management requires immediate decisions, and the available possibilities for endovascular therapy should always be considered.