Neck and Thoracic Outlet





Key Words:

carotid , vertebral , subclavian , neurologic , computed tomography angiography (CTA) , endovascular

 




Introduction


Vascular trauma to the neck and thoracic outlet may result in a catastrophic neurologic deficit or death if not recognized and properly treated. The spectrum of vascular injuries ranges from obvious life-threatening injuries that require immediate treatment to subtle injuries that may appear innocuous on initial examination and yet lead to a major neurologic event. This wide variation in presentation and potentially devastating nature of certain neck and thoracic outlet vascular injuries has led to a reappraisal of methods of diagnoses, imaging, and surgical management. These refinements have prompted changes in the management paradigm for both penetrating and blunt neck- and thoracic-outlet vascular injuries.


The surgical management of carotid artery injuries dates back to the 1500s. In 1552, Ambroise Paré authored the first report of successful management of a carotid artery injury by ligation. Both the common carotid artery and the jugular vein were ligated. The patient survived but developed aphasia and hemiplegia. Fleming later reported a successful outcome after ligating an injured common carotid artery, and this became the standard for surgical management until the Korean War. The Korean War marked the beginning of primary repair of arterial injuries, and carotid repair was attempted with success. Subsequently, these reconstructive techniques were applied to civilian carotid artery injuries as well as to the subclavian and, to a lesser extent, to the vertebral artery. More recently, endovascular techniques have replaced operative repair for selected injuries of the neck and thoracic outlet vessels.




Indications


Patients with either penetrating or blunt neck/thoracic outlet vessel injury frequently have severe concomitant injuries as well as nonvascular injuries remote from the site of injury. Therefore, a careful application of ATLS protocol for stabilization and treatment is crucial. Initial examination should include a thorough neurologic examination, auscultation for bruit, and palpation of the carotid and superficial temporal pulses. Upper extremity pulses and blood pressure in both arms should be evaluated, because pressure differentials or decreased pulses may suggest an arch or thoracic outlet injury.


Patients with carotid injuries may exhibit a contralateral neurologic deficit, aphasia, Horner’s syndrome, or evidence of anterior neck soft tissue trauma. Vertebral artery injuries may be associated with ataxia, dizziness, vomiting, facial and body analgesia, or visual field deficit. Complaints of headache, neck, ear, face, or periorbital pain may indicate mural hemorrhage or dissection. Because of the high association of blunt carotid and vertebral injuries with closed head injury, many patients have a decreased Glasgow Coma Scale (GCS) on arrival, which can complicate the diagnostic process. Patients with blunt carotid/vertebral injuries may also arrive at the emergency department (ED) with minimal to no overt vascular findings and yet develop a focal neurologic deficit 10 to 72 hours later. Penetrating subclavian artery injuries are particularly lethal. Of the patients who survive to reach the hospital, over half are hypotensive and require resuscitative thoracotomy. A pulse may be present distally despite significant arterial injury due to the robust collateral circulation of the shoulder. A brachial plexus injury accompanies a subclavian arterial injury in a third of patients and is a major cause of postoperative morbidity. First rib fractures are frequently associated with a blunt subclavian artery injury.


Physical examination is extremely important in the evaluation of penetrating injuries. Multiple studies have confirmed serial physical examination to be of value in the diagnosis of carotid injuries requiring repair, particularly zone II injuries. In addition, a negative physical examination decreases the likelihood of significant carotid injury in zone I and III ( Fig. 13-1 ) Available literature documents that the use of serial physical examinations provides a sensitivity of greater than 95% for detecting penetrating injuries that require repair.




FIGURE 13-1


Carotid zones of the neck. Zone I extends from the sternal notch to the cricoid cartilage. Zone II extends from the cricoid cartilage to the angle of the mandible. Zone III extends from the angle of the mandible to the base of the skull.


Because most blunt carotid and vertebral injuries are clinically occult, computed tomography angiography (CTA) or catheter-based angiographic screening of patients at risk for blunt vascular injuries of the neck is recommended. Patients at risk for blunt carotid/vertebral injury include those with: (a) head and neck trauma associated with severe neck hyperextension and rotation or hyperflexion; (b) a Lefort II or III fracture; (c) a basilar skull fracture involving the carotid canal; (d) a closed head injury consistent with diffuse axonal injury presenting with GSC score <6; (e) a cervical vertebral body or transverse foramen fracture, subluxation, or ligamentous injury at any level or any fracture of C1-C3; (f) a seat-belt or other clothesline-type injury with significant cervical pain, swelling, or altered mental status.


Most penetrating carotid injuries in neurologically intact patients should be repaired. In patients with a neurologic deficit, definitive repair should also be performed although controversy has existed in the past over vascular repair in this setting. In the 1970s, Cohen and Bradley raised the concern that repair of a carotid injury in a patient with a neurologic deficit may lead to intracranial hemorrhage. However, later studies by a number of authors conclusively demonstrated that regardless of the initial neurologic deficit, mortality and final neurologic status was improved overall if carotid repair was performed. Relative contraindications to repair include surgically inaccessible lesions, a delay of more than 3 to 4 hours from establishment of coma, large areas of cerebral infarct on admission MRI or CT studies and absence of retrograde back-bleeding from the distal arterial segment after operative exposure and open thrombectomy.


Nonoperative management of neurologically intact patients with specific penetrating injuries is occasionally warranted. For patients with a carotid or vertebral artery occlusion and normal neurologic exam, observation and anticoagulation with heparin is an acceptable approach. Likewise, patients diagnosed with a minimal arterial injury do not require repair. Minimal injuries are defined as nonobstructive or adherent intimal flaps and pseudoaneuryms less than 5 m in size. The safety of observation in minimal penetrating arterial injuries has been documented with data and follow-up extending to 10 years.


The indications for repair of a blunt carotid artery injury depend on the grade of injury on CTA or catheter-based angiography as follows: grade I, intimal injury with less than 25% luminal narrowing; grade II, dissection or hematoma with >25% luminal narrowing; grade III, pseudoaneurysm; grade IV, occlusion; and grade V, vessel transection. For patients initially managed nonoperatively, a follow-up CTA or catheter-based angiogram is recommended in 7 to 10 days because over 60% of injuries will change in grade or severity during this time interval. This is particularly true for grade I and II blunt injuries which often develop into grade III pseudoaneurysms. Additionally imaging 3 to 6 months after the injury is warranted in these cases to exclude the development of a pseudoaneurysm over time.


Fabian first demonstrated that anticoagulation improved survival (p < 0.02) and neurologic outcome (p < 0.01) in patients with blunt carotid injuries. Subsequent studies have also documented a trend toward improved neurologic outcome for asymptomatic patients undergoing antithrombotic therapy. Antithrombotic therapy for treatment of cervical arterial injuries consists of either therapeutic anticoagulation with heparin followed by Coumadin, or antiplatelet therapy with aspirin or aspirin plus clopidogrel. A recent Cochrane meta-analysis of antiplatelet therapy versus anti­coagulation therapy for carotid dissection showed no significant differences in stroke rate or hemorrhagic complications between these two medical treatment regimens. However, dual antiplatelet therapy may be preferred due to its safety and cost profile.


Current recommendations are that patients with grade I and II blunt carotid injuries be treated with antithrombotic therapy. Surgically accessible grade III injuries should be repaired. Inaccessible grade III injuries, which are often the scenario, should be managed by a covered stent or bare-metal stent combined with coil placement within the aneurysm ( Fig. 13-2 ). Grade IV injuries should be treated with antithrombotic therapy. Grade V injuries are frequently associated with nonvascular injuries and may require operative intervention as a life-saving maneuver. These injuries should be surgically repaired, if possible, but in most instances they require ligation or embolization due to their location. In patients with a blunt carotid injury for which endovascular repair is being considered, repair should be delayed for at least 7 days because earlier intervention is associated with a higher risk of stroke.




FIGURE 13-2


A, Angiogram of right internal carotid artery pseudoaneurysm due to a shotgun blast to zones II and III. The arrow points to the pseudoaneurysm. B, Completion angiogram following endovascular treatment with a bare-metal stent and coiling (arrow) of the pseudoaneurysm.


The natural history of blunt vertebral artery injury demonstrates that 90% of stenotic lesions will resolve and that 67% of occluded vessels will recanalize with antithrombotic therapy only. Both anticoagulation with heparin followed by Coumadin or antiplatelet therapy with aspirin or aspirin and Plavix have been utilized. Both regimens appear to have similar outcomes, and the optimal medical treatment for these injuries is yet to be determined. Blunt vertebral artery injuries tend to occur at junctions between fixed and mobile segments. The V2 segment is most commonly affected in adults whereas the V3 and upper V2 segments are more commonly affected in children ( Fig. 13-3 ). Approximately one third of patients have bilateral injuries. The need for operative intervention or endovascular repair is rare for both blunt and penetrating vertebral artery injuries.




FIGURE 13-3


Anatomic segments of the vertebral artery. V1 is from the subclavian origin to the entry into the C6 transverse foramen. V2 is from the C6 transverse foramen to the exit from the bony canal at the transverse process of C2. V3 is the extracranial segment between the transverse process of C2 and the base of the skull. V4 is the intracranial segment, terminating at its junction with the contralateral vertebral artery.




Preoperative Preparation


The preoperative preparation of patients with a documented neck and thoracic outlet vascular injury depends on the presence of active bleeding and the suspected location or zone of injury. Patients who are actively bleeding or have an expanding hematoma should go directly to the operating room (OR) for exploration, vascular control, and repair. In these instances, rapid establishment of an oral or nasotracheal airway is critical, especially for zone II penetrating injuries. Patients without evidence of bleeding and in whom a suspicion of a vascular injury exists require expeditious diagnostic imaging and, in select circumstances, require formal catheter-based diagnostic angiography. This approach is especially applicable for patients with zone I and III injuries in which access to the vessels in question is difficult. Although traditional teaching was that operative exploration of all penetrating zone II injuries is the best approach, evidence now shows that, in the absence of hemorrhage, initial CT imaging of this injury pattern is safe and may reduce the number of negative explorations. Duplex ultrasonography, if available in the ED, is particularly valuable in providing a quick, accurate assessment of zone II neck and thoracic outlet vasculature. Attention to and prioritization of associated nonvascular injuries is essential. Patients with a lateralizing neurologic deficit or altered mental status require a head CT or MR scan before operative intervention.


In most institutions, CTA is employed as the definitive diagnostic test. CTA findings, particularly for penetrating injuries, have been shown to be quite accurate and may be used as the basis for operative intervention. CTA is less accurate for blunt carotid and vertebral injuries. Recently published recommendations specify that a 16-slice or higher CTA is required for assessment of a possible blunt vascular injury. However, subsequent studies have documented a sensitivity of 29% to 64% and 51% to 54% with 16-slice and 64-slice scanners, respectively. Most blunt trauma patients receive a CT scan of some portion of their body, so adding a CTA of the neck is easily accomplished. A low threshold for the use of angiography should exist in patients at risk for blunt vascular injury. Depending on the mechanism, location, and type of injury, endovascular intervention at the time of diagnostic angiography may be the appropriate and definitive treatment.




Pitfalls and Danger Points





  • CTA and catheter-based angiography: For stable patients without evidence of hemorrhage, it is mandatory that a CTA or a catheter-based angiogram be performed before operative intervention in order to demonstrate the extent and the zone of injury. This information guides the surgical field and exposure required for proximal control.



  • Blunt carotid/vertebral injuries: Most of these injuries are best managed by antithrombotic therapy with either heparin followed by Coumadin or by antiplatelet therapy. Dual antiplatelet therapy may be preferable due to a better safety and cost profile. Failure to screen for these injuries and failure to treat with antithrombotic therapy increase the risk of neurologic deterioration and long-term morbidity.



  • Exit and entry wounds: Although an exit or entry wound may be in a zone or segment of a neck/thoracic outlet artery that is surgically accessible, the course and trajectory of the penetrating object should be considered when preparing the operative field. The surgeon must anticipate the need for more proximal or distal exposure depending on the trajectory and the course of the penetrating object.



  • Neurologic deficit: Careful neurologic examination of patients with a suspected or known carotid/vertebral injury is essential. Documentation of neurologic status before any intervention is critical to anticipating and recognizing new neurologic changes postoperatively.



  • Associated aerodigestive injuries: For neck arterial injuries, aerodigestive tract violations must be anticipated and investigated before arterial repair. If present, protection of the arterial repair by the interposition of muscle between the arterial repair and aerodigestive tract injury is mandatory.



  • Brachial plexus injury: The brachial plexus is frequently injured with thoracic outlet injuries. Consequently, a careful preoperative neurologic examination of the affected extremity is important to establish the degree of neurologic compromise. This allows for detection of new neurologic deficits postoperatively due to operative trauma or due to the development of an upper extremity compartment syndrome.



  • Proximal vascular control: Essential to successful repair and minimization of blood loss is proximal control of the artery before exposure of the injury. This is particularly important for proximal subclavian injuries and zone I carotid injuries, where either a median sternotomy, a proximal endovascular balloon occlusion or, in the case of a left subclavian artery injury, a third–fourth interspace left thoracotomy may be required. The proximal left subclavian artery cannot be controlled through a median sternotomy.



  • Venous injuries: Venous injuries are frequently associated with neck/thoracic outlet arterial injuries. In most patients ligation is appropriate and contributes to minimal morbidity. The more proximal the injury, the greater the likelihood that the venous injury requires operative repair. In the setting of bilateral internal jugular vein injuries, repair of one is advisable to prevent intracranial venous hypertension.



  • Cranial and phrenic nerves: The anatomic relationship of these nerves to the vasculature of the neck and thoracic outlet place them at risk during exposure and repair. Identification and preservation are important to minimize short- and long-term neurologic morbidity.



  • Internal carotid repairs: Thrombosis of the internal carotid artery due to either a blunt or penetrating injury may extend intracranially. Gentle passage of a thrombectomy catheter from the cervical carotid may be necessary to evacuate distal internal carotid thrombus. In the absence of back-bleeding, repair and reperfusion of the distal internal carotid should not be performed. In patients for whom back-bleeding is restored, intraoperative angiography should be used to document complete evacuation of all distal thrombus before repair and reperfusion.



  • Avoidance of hypotension and hypoxia: For patients with a neurologic deficit secondary to cortical brain injury, maintenance of normotension and avoidance of hypoxemia are essential to preserve the ischemic penumbra surrounding the cortical injury. Failure intraoperatively and postoperatively to maintain normotension and adequate oxygen saturation can extend the brain injury with subsequent neurologic deterioration.





Operative Strategy and Technique


Carotid


In 1969, Monson divided the neck into three zones ( Fig. 13-1 ). The zones of the neck were devised for guidance in diagnosis and treatment of carotid artery trauma. Zone I spans from the clavicle to the cricoid cartilage, zone II from the cricoid cartilage to the angle of the mandible, and zone III from the angle of the mandible to the skull base. The zone II carotid artery travels within the carotid sheath, which contains the vagus nerve and the jugular vein. The common carotid artery divides into the internal and external carotid within Zone II, in most instances one to two fingerbreadths below the angle of the mandible. An awareness of carotid bifurcation anatomy is important in preoperative planning, particularly for those injuries at the junction of zones II and III. It is also important to recognize that the zone classification describes the entry or exit site of the wound only. The course of a penetrating wound may traverse other zones of the neck or the thorax or intracranially.


The operative field for repair of a carotid injury requires surgical preparation of the neck and chest as well as a thigh for saphenous vein harvest. Carotid injuries in zone I and zone III are surgically challenging to access. For patients with a zone I carotid injury, median sternotomy may be required for proximal control. If the capability exists, endovascular techniques such as proximal arterial balloon occlusion can be used to establish rapid control of bleeding and to minimize the need for sternotomy. As shown in Figure 13-4 , if sternotomy is required, longitudinal extension along the anterior border of the ipsilateral sternocleidomastoid provides excellent exposure of the cervical carotid. Opening of the carotid sheath and retraction of the internal jugular vein laterally expose the common carotid artery. Care should be taken to identify and protect the vagus nerve within the carotid sheath.




FIGURE 13-4


A, Operative photograph of a left zone I common carotid artery repair performed with a reversed greater saphenous vein interposition graft. B, Note the position of the left common carotid origin posterior to the innominate artery on the aortic arch. In this approach, which was through a median sternotomy extended proximally in continuity with a left longitudinal cervical incision, the left subclavian artery origin is not visible.


For zone II injuries the facial vein, which typically is located at the carotid bifurcation, should be ligated and divided allowing for lateral retraction of the internal jugular vein and exposure of the cervical carotid artery. Cephalad dissection along the medial edge of the internal jugular vein exposes the proximal internal carotid artery. Dissection along the lateral border of the internal carotid artery exposes the hypoglossal nerve, which courses transversely across the superficial surface of the internal and external carotid arteries. Identification of this important nerve is facilitated by following the ansa hypoglossi nerve to its junction with the hypoglossal trunk.


More distal exposure of the internal carotid artery at the junction of zones II and III may require division of the occipital artery and mobilization of the posterior belly of the digastric muscle by release of its posterior fascial investment. Care should be taken to identify and preserve the glossopharyngeal and spinal accessory nerves, which typically lie behind the muscle fibers of the posterior belly of the digastric muscle and are at risk during zone III exposure. Anterior displacement of the mandible with fixation by intraoral wires may provide additional exposure but requires preoperative planning as well as establishment of a nasotracheal airway. This maneuver expands the base of the operative field from a narrow- to wider-based triangle, allowing 1 cm to 2 cm of additional exposure along the internal carotid artery. Alternative techniques such as mandibular subluxation and osteotomy impart little additional advantage and are associated with greater morbidity. A preoperative cervical and cerebral angiogram is essential to successful operative treatment of zone III neck injuries.


Arterial repair involves securing proximal and distal control, followed by exposure of the injured segment. A 2 or 3 French Fogarty™ balloon thrombectomy catheter should be passed gently both proximally and distally to remove thrombus. It is important to use an appropriately small thrombectomy catheter and to not overinflate the balloon in the internal carotid artery in order to avoid arterial spasm, thrombosis or perforation. Both proximal and distal arterial lumens should be flushed with heparinized saline solution (1000 units heparin/1 L saline); and systemic heparin, if not contraindicated, should be administered to decrease the risk of thrombosis and clot propagation. Intraluminal temporary vascular shunts such as the Sundt or Argyl rapidly reestablish prograde arterial flow and should be used for zone II internal carotid artery or carotid bifurcation injuries. Proximal common carotid injuries can be repaired without the use of a shunt in most instances.


The type of repair is dictated by the extent of injury. Primary repair or patch angioplasty is possible if the injury is a simple, small laceration as might occur with a stab wound. For more extensive injuries, it is important to identify and débride the injured arterial segment back to normal artery. Repair of more extensive injuries will require either an end-to-end anastomosis, an interposition graft or, when adjacent soft injury is extensive, a bypass graft. If necessary, an autogenous repair with a vein graft is recommended, particularly in the presence of aerodigestive tract injuries. However, prosthetic grafts can be utilized if needed, especially for common carotid injuries. For proximal internal carotid injuries, transposition of the external carotid to internal carotid provides another option when autogenous conduit is not available ( Fig. 13-5 ). Zone III internal carotid artery injuries may extend to the skull base, thereby precluding direct operative repair. In this situation, depending on the type of injury, nonoperative management or an endovascular approach may be the better option. In selected circumstances, ligation may be necessary; but this is associated with a high incidence of stroke. All completed repairs should be tension free and covered by viable soft tissue. Intraoperative completion arteriography or duplex scanning is mandatory to document technical perfection of the vascular repair and patency of distal arterial segments. Figure 13-2 depicts a successful endovascular treatment of an internal carotid artery pseudoaneurysm caused by a gunshot wound to zones II and III of the neck.




FIGURE 13-5


Illustration of external carotid–internal carotid transposition. A, Proximal ICA injury is depicted in. B, Transposition is accomplished by proximal mobilization of ECA with transposition and end-to-end anastomosis of the proximal ECA and ICA distal to the injury.


Endovascular management permits repair of injuries that are difficult or impossible to surgically expose (distal zone III) or lesions that would require extensive operative exposure (proximal zone I). Initially used for treatment of small arteriovenous fistulas and short-segment dissections, covered and uncovered stents are being used for more significant injuries as the technology improves and as experience is accrued. Endovascular treatment of carotid injuries should be considered, especially in high-risk patients with multiple concomitant injuries. Vascular access can be achieved with a femoral approach and with the use of long (>70 cm) sheaths or guide catheters. An array of small- to medium-sized covered and uncovered stents are now commercially available to manage proximal and distal injuries. As more ORs are transformed into high-resolution fluoroscopic units and surgeons become more adept in endovascular treatment modalities, the endovascular management of traumatic carotid injuries is certain to expand.


For zone III injuries not amenable to open or endovascular repair, proximal ICA ligation and extracranial–intracranial bypass can be considered. The outcome of carotid ligation alone for selected zone III injuries can be predicted based on preligation provocative temporary balloon occlusion testing. In patients who remain neurologically intact, ligation alone is acceptable with extracranial–intracranial bypass reserved for those who develop a deficit.


Vertebral


The vertebral artery arises as the first branch of the subclavian artery, usually at the C6-C7 level. In up to 6% of individuals, the left vertebral artery arises directly from the arch of the aorta between the origins of the left common carotid and left subclavian arteries. The vertebral artery is divided into four anatomic segments ( Fig. 13-3 ). V1 spans from the origin until entry into the C6 transverse foramen. The V2 segment extends from entry into the C6 transverse foramen until exit from the transverse process of C2. V3 is the extracranial segment between the transverse process of C2 and the base of the skull. V4 describes the intracranial segment, beginning at the entrance to the foramen magnum and terminating at the junction with the contralateral vertebral artery, by which the basilar artery is formed. The redundancy of the vertebral circulation is unique and permits the ligation of an injured, nondominant vertebral artery if necessary. Unilateral hypoplasia of the vertebral artery occurs in approximately 10% of individuals and can be identified on preoperative CT or catheter-based angiography.


Management of a vertebral artery injury depends on which anatomic segment is injured and on the condition of the contralateral vertebral artery. Vertebral arteries are more difficult to surgically access than the carotid artery, making direct surgical repair challenging. Consequently, for most penetrating or blunt injuries, regardless of the segment injured, ligation, embolization or nonoperative management is appropriate. When considering a nonoperative or ablative approach to an injured vertebral artery, it is important to determine, if possible, which of the vertebral arteries is larger or dominant. If it is determined that the injured artery is the dominant vertebral artery, a greater need to attempt a repair (e.g., endovascular stent or open revascularization) is indicated. In selected circumstances, depending on the quality of imaging and the location of the injury, it may not be possible to determine which vertebral artery is dominant or to attempt or complete a repair on the dominant vertebral artery injury. In such cases ligation or embolization of the artery, thus accepting a higher risk of posterior circulation stroke, is acceptable. Stents or embolization using coils, detachable balloons, liquid tissue adhesives, and other hemostatic agents have been used for pseudoaneurysms and selected arteriovenous fistulas. Most vertebral artery occlusions require antithrombotic therapy. Indications for operative management of a vertebral artery injury include patients with active hemorrhage and those who have failed endovascular management.


For the rare blunt or penetrating injury requiring open surgical repair, exposure of the V1 segment of the vertebral artery is via a medial transverse supraclavicular incision over the two heads of the sternocleidomastoid. Dividing the heads or splitting the two heads longitudinally exposes the carotid sheath. Opening the sheath, retracting the carotid medially, retracting the vagus nerve and internal jugular vein laterally, and dividing the vertebral vein directly posterior allows direct access to the vertebral artery and proximal subclavian artery.


Exposure of the V2-V5 segment of the vertebral artery is rarely necessary and is extremely challenging. The V2 segment requires exposure through the bony transverse foramina. Through the same exposure discussed for the V1 segment, the longus coli muscle is encountered in the deep posterior aspect of the neck. Once this muscle is swept off of the underlying bony structure, the anterior tubercle of the transverse process and the vertebral bodies are visualized. A bone rongeur is used to remove the anterior rim of the vertebral foramen to expose the vertebral artery. Moderate to severe bleeding may occur during this part of the dissection due to the venous plexus of the bony canal. Care should be taken not to injure the cervical nerve roots, which lie directly posterior to the artery. A posterior auricular approach is required to expose the V3 segment of the artery, and the V4 segment can only be exposed with a craniotomy. Exposure of V3 and V4 segments is best done with the assistance of a neurosurgeon.


Subclavian


The left subclavian artery arises as the third and final great vessel from the aortic arch. The right subclavian artery arises from the innominate artery. The subclavian artery extends from its origin to the lateral border of the first rib. It is divided into three segments based on the relationship of the anterior scalene muscle ( Fig. 13-6 ). The first portion, medial to the anterior scalene muscle contains the most important branches, including the vertebral artery, the internal mammary artery, and the thyrocervical trunk. The second segment lays posterior to the anterior scalene, and the short third segment extends from the lateral border of the anterior scalene muscle to the lateral edge of the first rib, where it becomes continuous with the axillary artery. The phrenic nerve lies either directly on or medial to the anterior scalene muscle and can be injured during exposure of the first and second segments of the artery. The artery anatomically is posterior to the subclavian vein, the vertebral vein, the anterior scalene muscle and the thoracic duct on the left.


Oct 11, 2019 | Posted by in CARDIOLOGY | Comments Off on Neck and Thoracic Outlet

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