Airgun injuries are prevalent in the pediatric population. The present study described a case of air gun pellet injury to the left carotid artery and its successful management. A 25-year-old man presented to the emergency department complaining that his son had accidentally injured him with an air gun pellet while playing. The X-ray cervical spine revealed a single foreign body (pellet) located directly anterior to the C5-C6 vertebra. A CT angiography of the neck showed a spherical hyperdense object just anterior to the C6 vertebral body on the left side, 3 mm posteromedial to the left common carotid artery, which was most likely a pellet foreign body. The patient was sent to operation theatre (OT) for exploration. There was a rent in the internal carotid artery with active bleeding. After exerting both proximal and distal control, the rent was closed. Close air gun injury could result in gunshot wounds, as in the present case. Plain X-rays in AP and lateral view are required. Nonoperative management could be employed in a restricted group of patients with satisfactory outcomes. Those who have vascular involvement will require surgical intervention.

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.

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.

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.

Life-threatening hemorrhage following maxillofacial injury (MFI) is rare but can be fatal. Conventional measures for hemostasis including nasal packing, balloon tamponade, and surgical ligation of bleeding points may not be effective or efficient in patients at risk of hypovolemic shock. Advantages of transarterial embolization (TAE) include rapid identification of the bleeding focus and its access, direct obstruction of the culprit vessels, ability to control multiple bleeding sites, and no requirement of general anesthesia. The internal maxillary artery is the most frequently targeted vessel for embolization. Several studies have demonstrated that TAE was technically successful at rates between 79.4% and 100% and was associated with good clinical outcomes. However, major complications such as tongue necrosis or facial nerve palsy have rarely been reported (0%-7%), probably because of rich collaterals in the maxillofacial region, and failure to diagnose complications in patients who are severely disabled or died. Traditionally, Gelfoam and coils have been widely used as embolic materials. Polyvinyl alcohol particles and n-butyl-cyanoacrylate are also favored, and newer embolic materials, such as Onyx or precipitating hydrophobic injectable liquid, are available for use. Operators should be familiar with the distinctive characteristics of each embolic material. Early treatment with TAE for intractable hemorrhage may improve outcomes in patients with MFI, and further studies are necessary to develop a treatment algorithm to define when to initiate TAE in cases of severe oronasal hemorrhage following MFI.

BACKGROUND: Carotid artery pseudoaneurysm (PSA) is infrequently encountered in clinical settings. Internal carotid artery (ICA) PSA complicated with ischemic stroke is rare. PSAs are typically caused by iatrogenic injury, trauma, or infection. The underlying mechanisms of spontaneous PSA formation are not well characterized. We report a healthy young man who presented with stroke as a complication of spontaneous PSA of the left ICA.
METHODS: A 30-year-old man working as a ceiling decoration worker was hospitalized due to sudden-onset speech disorder and right lower extremity weakness. Medical history was unremarkable. Brain computed tomography revealed ischemic stroke. Digital subtraction angiography showed a left ICA PSA with mild stenosis. The patient was conservatively managed with oral anticoagulation and antiplatelet therapy. He recovered well and was discharged. The patient was in good condition during follow-up.
CONCLUSIONS: The occupational history of patient should be taken into consideration while evaluating the etiology of spontaneous ICA PSA in young people with stroke.

A 49-year-old patient with a history of aspirin-exacerbated respiratory disease presented with carotid artery injury following revision functional endoscopic sinus surgery. Carotid artery injury is a rare but catastrophic complication of this surgery. The patient was transferred to our tertiary facility with interventional radiology for immediate management of the carotid artery injury. This case reaffirms that any surgery can have disastrous complications and highlights the importance of multidisciplinary management of complications such as carotid artery injury.

Carotid body tumor excision can lead to various complications including vascular injury and pseudoaneurysm formation. Here we describe a case of carotid body tumor excision followed by series of complications including pseudoaneurysm formation, failure of primary surgical repair, carotid stump syndrome following parent artery occlusion, and persistent hypotension.