UNASSIGNED: In penetrating neck trauma, carotid artery penetrating trauma is considered one of the most complicated injuries to treat. Active bleeding, large hematomas, and rapid occlusion of the airways make the surgical approach to controlling bleeding and repairing the vessel much more complex, constituting an essential clinical challenge to every surgeon.
METHODS: We present 4 cases of patients with carotid artery penetrating trauma. Two patients were treated with endovascular therapy, one with surgery, and the fourth one treated conservatively. None of the patients had posterior neurological impairment.
UNASSIGNED: Carotid artery penetrating trauma is uncommon yet is associated with high rates of mortality and neurological impairment. The common carotid artery is the most frequently injured, and gunshot wounds (GSW) are the most frequent trauma mechanism. Angiotomography (CTA) is the first-line exam for diagnosing these injuries. Treatment should be prompt and individualized and may include conservative techniques, endovascular therapy, and traditional surgical repair.
CONCLUSIONS: Carotid artery penetrating trauma is an uncommon but complex injury that requires a timely diagnosis and treatment to avoid potentially devastating consequences, particularly in hemodynamically unstable patients. Traditionally, the treatment strategies for these injuries used to be limited to vascular repair or ligation. However, endovascular therapy and conservative management are viable alternatives, which have become more and more useful in selected patients, allowing less invasive approaches with fewer morbidity and acceptable results.

Identification of vascular injuries is crucial for complete postmortem evaluation and understanding of trauma deaths by the Medical Examiner. Some vascular injuries are difficult to evaluate due to challenging anatomic locations, especially in the head and neck. Documenting injuries of the facial and vertebral arteries is challenging and necessitates time-consuming dissections that can create artifacts and disfigurement. In busy medical examiner offices with a significant number of traumatic injuries, finding a creative solution to employ reliable postmortem angiography is desirable. At the Office of the Chief Medical Examiner for the State of Maryland (OCME), we created and effectively implemented a selective angiography procedure using traditional indwelling Foley catheters and water-soluble barium swallow contrast to evaluate arterial injuries using either digital radiography or computed tomography imaging modalities. This technique and imaging interpretation can be performed by a medical examiner or forensic pathology fellow after basic technical training and basic radiology training. This study outlines the technique, methods, and utilization of the procedure and describes the findings of six deaths due to vascular lesions from different injury mechanisms and disease processes and describes the ease of implementation on a broader scale in busy Medical Examiner\'s offices.

Among the various anatomical landmarks during neck dissection, digastric muscle is one of the most important. It is well known that all important blood vessels in neck lies deep to digastric. Thus, it acts as a safety landmark during neck dissection. In this article we describe a variation in vascular anatomy with relation to posterior belly of digastric that has not been reported so far during live surgery. Surgeon performing neck dissection should have a detailed knowledge of anatomy and infrequent anatomical variation. The knowledge of current anatomical variation will avoid torrential bleed during neck dissection and preserve the artery for vascular related procedures.

The study aims to explore the fluctuating expression of C/EBP Homologous Protein (CHOP) following rat carotid artery injury and its central role in vascular stenosis. Using in vivo rat carotid artery injury models and in vitro ischemia and hypoxia cell models employing human aortic endothelial cells (HAECs) and vascular smooth muscle cells (T/G HA-VSMCs), a comprehensive investigative framework was established. Histological analysis confirmed intimal hyperplasia in rat models. CHOP expression in vascular tissues was assessed using Western blot and immunohistochemical staining, and its presence in HAECs and T/G HA-VSMCs was determined through RT-PCR and Western blot. The study evaluated HAEC apoptosis, inflammatory cytokine secretion, cell proliferation, and T/G HA-VSMCs migration through Western blot, ELISA, CCK8, and Transwell migration assays. The rat carotid artery injury model revealed substantial fibrous plaque formation and vascular stenosis, resulting in an increased intimal area and plaque-to-lumen area ratio. Notably, CHOP is markedly elevated in vessels of the carotid artery injury model compared to normal vessels. Atorvastatin effectively mitigated vascular stenosis and suppresses CHOP protein expression. In HAECs, ischemia and hypoxia-induced CHOP upregulation, along with heightened TNFα, IL-6, caspase3, and caspase8 levels, while reducing cell proliferation. Atorvastatin demonstrated a dose-dependent suppression of CHOP expression in HAECs. Downregulation of CHOP or atorvastatin treatment led to reduced IL-6 and TNFα secretion, coupled with augmented cell proliferation. Similarly, ischemia and hypoxia conditions increased CHOP expression in T/G HA-VSMCs, which was concentration-dependently inhibited by atorvastatin. Furthermore, significantly increased MMP-9 and MMP-2 concentrations in the cell culture supernatant correlated with enhanced T/G HA-VSMCs migration. However, interventions targeting CHOP downregulation and atorvastatin usage curtailed MMP-9 and MMP-2 secretion and suppressed cell migration. In conclusion, CHOP plays a crucial role in endothelial injury, proliferation, and VSMCs migration during carotid artery injury, serving as a pivotal regulator in post-injury fibrous plaque formation and vascular remodeling. Statins emerge as protectors of endothelial cells, restraining VSMCs migration by modulating CHOP expression.

BACKGROUND: Vertebral artery injury is a rare condition in trauma settings. In the advanced stages, it causes death.
METHODS: 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.

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.

CNS injury following a traumatic intraoral injury is a rare but potentially catastrophic occurrence in pediatrics. For example, intraoral trauma resulting in acute ischemic stroke (AIS) secondary to carotid artery dissection has only been described by a limited number of case reports [1]. We report the case of a 4-year-old boy who suffered a penetrating right internal carotid injury after a fall resulting in a metal straw perforating the neck and oropharynx. The patient presented in hemorrhagic shock with altered consciousness. CT Angiography revealed a right internal carotid traumatic rupture with flow occlusion and right cerebral hemispheric hypoperfusion. The patient underwent emergent neuroradiologic intervention under general anesthesia with successful reconstruction of the right carotid artery through the use of five flow diverting pipeline stents. The patient was extubated one week later with the only neurologic sequala being slight left upper extremity weakness. Anesthetic management played a vital part in this outstanding outcome. Thoughtful management is required to ensure both survival and the best possible neurologic recovery. Despite the rarity of these events, there is sufficient evidence from similar interventions and neurophysiology to guide sound management. This case report highlights these principles and areas for further investigation. Our experience may be instructive in the support of safe care under similarly rare but challenging circumstances.

Prior studies have demonstrated a close association between cervical spine fractures and blunt cerebrovascular injuries (BCVI). Undiagnosed BCVI is a feared complication because of the potentially catastrophic outcomes in a missed posterior circulation stroke. Computed tomography angiography (CTA) is commonly used to screen BCVI in the trauma setting. However, determining which cervical fracture patterns mandate screening is still not clearly known.
The aim of this retrospective review is to further elucidate which fracture patterns are associated with BCVI when using CTA and may mandate screening.
Retrospective cohort study.
All patients that presented to our trauma and emergency departments with a blunt cervical spine fracture from January 2018 to December 2021. Inclusion criteria included blunt cervical trauma and the use of CTA for BCVI screening. Exclusion criteria included patients under the age of 18, penetrating cervical trauma, and use any imaging modality besides CTA for BCVI screening.
Patient demographics (age, gender, Glasgow coma scale, hospital length of stay (LOS), intensive care unit LOS, mechanism of energy of injury, polytrauma status), fracture location, fracture pattern (anterior arch, dens, dislocations/subluxations, facet, hangman, Jefferson, lamina, lateral mass, occipital condyle dissociation, occipital condyle, pedicle, posterior arch, spinous process, transverse process, transverse foramen, and vertebral body), and whether the patient sustained a BCVI or CVA.
If a patient had multiple fracture levels or fracture patterns, each level and pattern was counted as a separate BCVI. Multilevel fractures were defined as any patient with fractures at two distinct cervical levels. Differences between the patients who had a BCVI and those who did not were analyzed using independent sample t-tests for continuous variables and the chi-square or Fisher exact test for categorical variables. Odds ratios and 95% confidence intervals were calculated to assess likelihood between patient characteristics/fracture characteristics and BCVI.
A total of 690 patients were identified as having a blunt cervical spine injury. A total of 453 patients (66%) underwent screening for BCVI with CTA. Among patients who underwent CTA, BCVI was diagnosed in 138 patients (30%), VAI in 119 patients (26%), CAI in 30 patients (7%), and 11 patients were diagnosed with both a VAI and CAI (2%). Overall, among all patients there were 9 strokes, all in patients identified with a BCVI (1%). No individual cervical level was associated with increased risk of BCVI, but when combined, OC-C3 fractures were associated with an increased risk (OR: 1.4, 95% CI: 1.0-1.9, p-value: .006). Multilevel fractures were also associated with an increased risk (OR: 1.7, 95% CI: 1.1-2.3, p-value: .01). The only fracture pattern associated with increased risk of BCVI were fractures associated with a dislocation/subluxation (OR: 3.8, 95% CI: 1.9-7.8, p-value = .0001).
The only fracture pattern associated with an increased risk of BCVI were fractures associated with dislocation/subluxation. The only fracture levels associated with BCVI were combined OC-C3 and multilevel fractures. We recommend that any upper cervical fracture (OC-C3), multilevel fracture, or fracture with dislocation/subluxation undergo screening for BCVI.

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.

Invasive pituitary adenomas can infiltrate the dura mater, sphenoid sinus, or cranial bone. Endoscopic transsphenoidal sinus surgery is considered the standard of care; however, several potential complications must be noted. These complications can include cerebrospinal fluid leaks, infection, bleeding, optic nerve damage, and endocrinological complications such as diabetes insipidus. We present a case of a 69-year-old female with multiple recurrent invasive pituitary adenomas who has previously undergone 5 transsphenoidal procedures. Intraoperatively, the patient suffered from a left-sided carotid artery injury that was repaired with a muscle graft. Management of carotid artery injury during transsphenoidal surgery is optimized in a step-by-step approach which includes early recognition of the injury, briefing the surgical team, immediate control using compression, use of additional tissue graft for wound repair, and postoperative care. Through the use of the approach mentioned above, we were able to control the complication successfully.