Neck and Thoracic Outlet

Introduction

Perhaps no other anatomic region contains so many vital structures in such a compact space as the neck and thoracic outlet. Injuries in this region can result in hemorrhage, stroke, upper and/or lower extremity paralysis, loss of airway, and digestive tract injury. Consequently, the clinician must adopt a thorough approach and maintain a high index of suspicion when caring for patients with injuries in this area. The spectrum of vascular trauma in the cervical region ranges from exsanguinating hemorrhage to subtle imaging findings with a seemingly innocuous examination that can lead to delayed hemispheric stroke. The variation in presentation and potentially devastating nature of neck and thoracic outlet injuries has led to an increased awareness and screening for patients with penetrating wounds and those at risk for blunt vascular injury.

The surgical management of carotid artery injuries dates back to 1552, when Ambroise Paré reported the successful management of a common carotid artery and jugular vein injury by ligation. The patient developed aphasia and hemiplegia but survived. Fleming later reported a favorable outcome after ligating an injured common carotid artery, and this became the standard surgical management until the Korean War. In his review of the management of arterial injuries during World War II, DeBakey found that arterial repair was associated with higher mortality rates, and based on this report, the US military abandoned arterial repair. Frank Spencer is credited with bringing back arterial injury repair during the Korean War with improved results, including injuries to the carotid. Subsequently, these reconstructive techniques were applied to civilian carotid and subclavian artery injuries. More recently, endovascular techniques have been applied to selected injuries of the neck and thoracic outlet vessels.

Indications

Patients with neck/thoracic outlet vessel injury frequently have concomitant injuries. The use of advanced trauma life support protocol is crucial to recognize and treat life-threatening injuries first and then thoroughly evaluate for other possible injuries. The secondary survey of the patient should include a neurologic examination, auscultation for bruits, and assessment of carotid and upper extremity pulses, and blood pressure in both arms. Pressure differentials or decreased pulses may suggest a thoracic outlet injury.

Patients with carotid injuries may present with contralateral extremity deficit, aphasia, or Horner's syndrome. Vertebral artery injuries rarely present with neurological symptoms, but posterior cerebral symptoms such as ataxia, dizziness, vomiting, facial and body analgesia, or visual field deficits mandate evaluation of their cerebral vasculature. Complaints of headache, neck, ear, face, or periorbital pain may indicate intramural hemorrhage or dissection. Because of the frequent association of blunt cerebrovascular injuries (BCVI) with closed head injury, many patients have a decreased Glasgow Coma Scale (GCS) on arrival, which makes physical examination–directed diagnosis a challenge. Patients with BCVI may also arrive at the emergency department (ED) with no neurological deficit and then develop a delayed neurologic deficit 10 to 72 hours later. Penetrating subclavian artery injuries are particularly lethal due to severe noncompressible hemorrhage with over half who survive to the hospital requiring resuscitative thoracotomy. More than a third of those who survive also have associated brachial plexus injuries, which cause significant postoperative morbidity.

Physical examination is extremely important in the evaluation of penetrating injuries, including the number, location, and possible trajectory of wounds. Hard signs of vascular injury are pulsatile hemorrhage, expanding hematoma, absent distal pulses, and palpable thrill, all of which mandate exploration. Soft signs include peripheral nerve deficit, significant hemorrhage at the scene, nonexpanding hematoma, and decreased distal pulse, which should be evaluated by computed tomography angiography (CTA) or other imaging modality. Minor vascular injuries do not always require repair and can be followed by serial physical examination with or without duplex ultrasound, an approach that has 95% sensitivity for detecting injuries that require repair.

Because most blunt cerebrovascular injuries are clinically occult, screening CTA of the neck should be performed on patients with risk factors such as: (1) head and neck trauma associated with severe neck hyperextension and rotation or hyperflexion; (2) a Lefort II or III fracture; (3) a basilar skull fracture involving the carotid canal; (4) a closed head injury consistent with diffuse axonal injury presenting with GCS score less than 6; (5) a cervical vertebral body or transverse foramen fracture, subluxation, or ligamentous injury at any level or any fracture of C1–C3; or (6) a seat-belt or other clothesline-type injury with significant cervical pain, swelling, or altered mental status.

Definitive repair of penetrating carotid injuries in patients with a neurologic deficit has been controversial. 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, subsequent studies found that regardless of the initial neurologic deficit, mortality and final neurologic status was improved if carotid repair was performed. A comprehensive review of the US military’s experience with cervical carotid injury during the wars in Afghanistan and Iraq showed that common and internal carotid artery repair resulted in lower rates of stroke and death when compared to ligation. 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 CT, and absence of retrograde back-bleeding from the distal arterial segment after operative exposure and open thrombectomy.

Nonoperative management of neurologically intact patients with penetrating injuries is occasionally warranted. For patients with a carotid or vertebral artery occlusion and normal neurologic examination, observation and anticoagulation with heparin is an acceptable approach. Likewise, minimal arterial injuries, defined as non–flow-limiting intimal flaps and pseudoaneurysms less than 5 mm in size, can be safely observed, based on series with follow-up extending to 10 years. These injuries should be evaluated by repeat CTA or duplex prior to discharge to confirm they have not progressed. The current grading system for BCVI is: grade I, intimal injury with less than 25% luminal narrowing; grade II, dissection or hematoma with more than 25% luminal narrowing; grade III, pseudoaneurysm; grade IV, occlusion; and grade V, vessel transection.

BCVI are almost always managed nonoperatively based on Fabian’s finding that antithrombotic therapy improved survival ( P < .02) and neurologic outcome ( P < .01) in patients with this injury pattern, a result that has been confirmed in several subsequent reports. Antithrombotic therapy consists of either therapeutic anticoagulation with heparin followed by warfarin, 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 differences in stroke rate or hemorrhagic complications between the two treatment regimens. However, dual antiplatelet therapy may be preferred due to its safety and cost profile. A follow-up CTA is recommended 7 to 10 days after injury because over 60% of injuries will change in grade or severity during this time interval. Grade I and II BCVI can 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 an enlarging pseudoaneurysm over time.

Current recommendations are that patients with grade I–IV BCVI 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 many instances they are surgically inaccessible and require ligation or embolization.

The natural history of BCVI is that 90% of stenotic lesions will resolve and that 67% of occluded vessels will recanalize with antithrombotic therapy only. Blunt vertebral artery injuries tend to occur at junctions between fixed and mobile segments with the V2 segment most commonly affected in adults, and the V3 and upper V2 segments more commonly affected in children. 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.

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 have hard signs of vascular injury should go directly to the operating room (OR) for exploration, vascular control, and repair. Rapid establishment of an oral or nasotracheal airway is critical. Patients with soft signs of vascular injury 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 surgical access to the vessels in question is difficult. Duplex ultrasonography can provide a rapid, accurate, and noninvasive assessment of zone II neck and thoracic outlet vasculature; however, it is often not available in the ED, whereas CTA has become the diagnostic evaluation of choice. CTA findings are accurate and may be used as the basis for operative planning. 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. Depending on the mechanism, location, and type of injury, endovascular intervention at the time of diagnostic angiography may be an appropriate and definitive treatment.