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Vascular Trauma: Head and Neck
Cervical vascular injuries are notoriously difficult to evaluate and to manage, mostly secondary to complex anatomy confined to a relatively narrow and layered anatomic space. The initial evaluation of these patients is often obscured by associated injuries to the head, chest, or abdomen. In addition, signs of cerebral ischemia, cranial nerve deficits, or cervical nerve compression may not be present on initial evaluation. The evaluation and appropriate management of these injury patterns have been controversial and continue to evolve. Advances in noninvasive imaging (primarily computed tomography) have revolutionized the evaluation of stable patients with cervical vascular injuries, aerodigestive injuries, and associated fractures. In addition, endovascular surgery has added another facet to the care of these trauma patients. Injuries to the distal internal carotid artery, proximal common carotid artery, subclavian artery, or vertebral arteries are now amenable to endovascular methods to arrest hemorrhage, to exclude dissections and pseudoaneurysms, or to assist with open repair. This chapter addresses the presentation, evaluation, and treatment of cervical vascular injuries.
Carotid Arteries
Penetrating Injury
After penetrating cervical trauma, cervical blood vessels are the most commonly injured structures in the neck and account for a 7% to 27% stroke rate and a 7% to 50% mortality. In this population, 80% of deaths are stroke related.
Clinical Presentation
The neck has classically been divided into three zones that dictate diagnostic evaluation and treatment ( Fig. 180.1 ):
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Zone I: below the cricoid cartilage – proximal control obtained in the chest.
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Zone II: between the cricoid cartilage and the angle of the mandible – proximal and distal control obtained in the neck.
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Zone III: above the angle of the mandible – distal control difficult to obtain.
Zone II is the most commonly injured (47%), followed by zone III (19%) and zone I (18%). It is not uncommon for the injury to traverse two zones of the neck. In addition to location, the physical examination triages patients on the basis of “hard signs” of vascular injury (mandating exploration) and “soft signs” of vascular injury (observation vs. further diagnostic evaluation). Hard signs include shock, refractory hypotension, pulsatile bleeding, bruit, enlarging hematoma, and loss of pulse with stable or evolving neurologic deficit. Soft signs include history of bleeding at the scene of injury, stable hematoma, nerve injury, proximity of injury track, and unequal upper extremity blood pressure measurements. Ninety-seven percent of patients with hard signs have a vascular injury as opposed to only 3% with soft signs.
On the basis of mechanism of injury, gunshot wounds are more likely to cause a large neck hematoma and vascular injury (27%) compared with stab wounds (15%). Shotgun wounds, blast injuries, and transcervical (crossing midline) gunshot wounds have a higher rate of vascular injury and should be approached with a high index of suspicion. Associated injuries to the tracheobronchial tree, esophagus, and spinal cord are present in 1% to 7% of patients. In addition to hard signs of a vascular injury, patients may present with hard signs of a tracheobronchial injury (respiratory distress or air bubbling from the wound), mandating operative exploration. Other soft signs of cervical neck injury include painful swallowing, subcutaneous emphysema, hematemesis, and signs of nerve injury (cranial nerves IX, X, XI, and XII) or brachial plexus injury (axillary, musculocutaneous, radial, median, and ulnar nerves). A focused and detailed clinical evaluation reliably identifies patients with vascular injuries that require treatment. A physical examination with normal findings has a negative predictive value of 90% to 100% for vascular injuries.
Special consideration should be given to patients who present with coma, a dense hemispheric stroke, or documented carotid thrombosis. The treatment of this specific injury pattern has come full circle from revascularization in the 1950s, to routine ligation in the 1970s, followed by revascularization as the current mainstay of treatment. In the 1970s, authors reported only a few patients with dense hemispheric stroke who developed hemorrhagic stroke after revascularization, leading to the recommendation of internal carotid artery ligation distal to the thrombus. Follow-up studies demonstrated that the extent of anoxic brain injury (not hemorrhagic conversion of the injury), development of reperfusion injury, cerebral edema, and resultant uncal herniation accounted for patients with worsening neurologic status and death. , However, to date, there is no preoperative marker other than time (>24 hours from time of injury) that predicts those patients unlikely to benefit from revascularization. Early revascularization has consistently demonstrated improvement or stabilization of neurologic symptoms in patients with dense hemispheric strokes (100%), even in patients who present obtunded (50%). ,
Diagnostic Evaluation
Patients with hard signs of a vascular injury should proceed to the operative suite. All patients should have plain radiographs of the neck and chest to determine the track of the injury and to diagnose occult hemothoraces or pneumothoraces. There have been several advances in the treatment of penetrating neck injuries, and data are now sufficient to support selective exploration in hemodynamically stable patients who do not have hard signs of a vascular or tracheobronchial injury. Exploration of cervical injuries based on platysma muscle penetration carries an unacceptably high negative exploration rate of 50% to 90%.
Computed tomography is the modern workhorse for trauma evaluation and should be the initial diagnostic step in evaluating patients with penetrating neck injuries who do not have hard signs of vascular or aerodigestive injury. Contrasted axial imaging with reformatting software allows exact determination of the injury track, vascular injuries, proximity to the esophagus and trachea, spinal fractures and cord involvement, and extension into the head or chest ( Fig. 180.2 ). In the setting of penetrating cervical injuries, computed tomographic angiography (CTA) has a 90% sensitivity and 100% specificity for vascular injuries that require treatment. , CTA may be limited secondary to missile fragments (especially shotgun injuries) or bone fragments obscuring the cervical vasculature; arteriography should be used for these patients as a confirmatory study. Ultrasonography has been used for penetrating neck trauma, but its utility is limited to zone II neck injuries. In addition, subcutaneous air, fragments, and hematomas make ultrasound less reliable.
Medical Treatment (Nonoperative Management)
Occult injuries (intimal flaps, dissections, and pseudoaneurysms) identified during evaluation for penetrating cervical injury should be managed just as those caused by blunt trauma (detailed later). Isolated intimal flaps are rare in penetrating trauma, and dissections occur in only 2% of cases. Pseudoaneurysms are the most common occult injury identified. Large pseudoaneurysms should be considered for early intervention, whereas small pseudoaneurysms should be treated with antithrombotic therapy and early follow-up imaging. The natural history of these lesions is not known; however, patients should be closely monitored for development of embolic symptoms.
Endovascular Treatment
An endoluminal approach to neck injuries may avoid the morbidity of median sternotomy, a high thoracic incision, or difficult dissection at the base of the skull. Another benefit is that endoluminal therapy can be performed under local anesthesia, allowing the provider direct assessment of the patient’s neurologic status. For zone I and zone III injuries, endovascular exclusion of a pseudoaneurysm, partial transection, or arteriovenous fistula remains a viable option based on the location of injury and the patient’s clinical status. Self-expanding covered stents can be safely delivered to these locations with limited morbidity. Zone II injuries should be approached with operative repair.
Surgical Treatment
Proximal and distal control in the neck
Obtaining control of the injury in each zone presents unique challenges. All patients should have their proximal thighs (potential vein conduit) and chest (potential proximal control) prepared into the operative field. Zone I injuries that are manifested with hard signs may be approached through a cervical incision, but a median sternotomy or high anterolateral thoracotomy will be required to obtain proximal control. If the patient is in shock, endovascular attempts at proximal control should not delay performing a median sternotomy. Depending on the patient’s hemodynamics and the location of injury, proximal control of the great vessels may be performed from a femoral approach in the operative suite with balloon occlusion (a large 33-mm compliant balloon catheter). Alternatively, if the proximal vessel can be visualized from a cervical approach but not secured with a vascular clamp, a compliant balloon or Fogarty catheter can be passed retrograde for temporary proximal control. Once the vessel is properly exposed, the balloon can be replaced with a vascular clamp.
An overt injury in zone II can be readily approached through a cervical incision and repair performed under direct visualization. The most common vessel injured by penetrating mechanisms is the internal jugular vein followed by the common carotid artery. The operative feasibility, ability to examine the aerodigestive tract, and relatively low risk to exploration in this region favor open exploration over endovascular techniques in emergent situations.
Hemorrhage from a zone III injury can be devastating, and an immediate operative exploration through a cervical incision can be used first to control inflow and to assess the injury pattern. Even after subluxation of the mandible and division of the posterior belly of the digastric muscle, the distal extent of the injury may not be visualized. If the vessel is transected with inadequate length for clamp application, distal control can be obtained by placing a Fogarty balloon (No. 3–4) within the vessel lumen. If the vessel is lacerated, a sheath can be placed in the common carotid artery and a Fogarty catheter can be passed antegrade through the injury to control back-bleeding. Once the Fogarty balloon is inflated, arteriography can be performed through the side arm of the sheath to delineate the injury with respect to the skull base and further guide operative exposure. Once hemorrhage is arrested, the surgeon must decide whether to proceed with operative repair, embolization of the carotid artery, endoluminal stenting, or temporary shunting or to return the patient to the intensive care unit for resuscitation, imaging of the brain, and delayed repair. If a damage control approach is used, the patient should have serial imaging to evaluate evolving cerebral edema, and cerebral perfusion pressures should guide further resuscitative maneuvers.
Surgical repair of cervical vessels
Once the injury has been delineated and controlled, the surgeon must decide whether to ligate, repair, or temporarily shunt the vessel. The internal jugular vein and external carotid artery may be ligated with limited morbidity. Ligation of the internal carotid artery results in a 45% mortality, and it should be reserved only for injuries at the base of the skull that are not amenable to reconstruction. Clean-based lacerations caused by stab wounds may be repaired primarily; however, gunshot wounds, fragmentation wounds, and shotgun injuries typically require reconstruction of the common carotid or internal carotid artery. Shunts should be used in patients who are already at risk of cerebral hypoperfusion secondary to shock and to all injuries of the internal carotid artery. If the distal clamp can be placed below the carotid bulb, the internal carotid artery will receive adequate back-bleeding through the external carotid artery. Heparin (50 units/kg) should be given before clamps are placed.
The greater saphenous vein has good size match with the internal carotid artery and when used as an interposition graft has demonstrated excellent patency and limited infectious risk. The external carotid artery can also be transposed to the internal carotid artery for injuries in the proximal internal carotid. In addition, superficial femoral artery can be used in the common or internal carotid artery but requires an additional reconstruction in the lower extremity with polytetrafluoroethylene (PTFE). PTFE typically has a better size match than the greater saphenous vein in the common carotid artery, and in this location, there is no difference in patency rates between the two conduits. In the setting of associated aerodigestive injuries, autogenous conduits should be used, the esophageal repair should be drained away from the vascular repair, and a muscle pedicle (cervical strap muscles, omohyoid muscle, digastric muscle, or sternal head of the sternocleidomastoid) should be placed between the two repairs.
After repair of the vascular injury, all patients must be monitored for signs of cerebral edema and intracranial hypertension. If a clinical neurologic examination cannot be performed, direct intracerebral pressure monitoring or serial head imaging should be obtained.
Blunt Cerebrovascular Injuries
The overall incidence of blunt cerebrovascular injury (BCVI) has been universally reported as less than 1% of all trauma admissions for blunt trauma, but this relatively small population of patients has stroke rates ranging from 25% to 58% and mortality rates of 31% to 59%. The variability in incidence of BCVI is 0.19% to 0.67% for unscreened populations compared with 0.6% to 1.07% for screened populations.
Clinical Presentation
The recognition and treatment of BCVI have dramatically evolved during the past 2 decades. As imaging technology has improved with respect to both image quality and acquisition times, its use has become a fundamental diagnostic tool in blunt trauma evaluation. Paralleling advances in noninvasive imaging, a heightened awareness of BCVI has emerged. Through aggressive screening, these injuries have increasingly been recognized before devastating neurologic ischemia results.
Mechanism of blunt cerebrovascular injury
Three basic mechanisms of injury are encountered: (1) extreme hyperextension and rotation; (2) a direct blow to the vessel; and (3) vessel laceration by adjacent bone fractures. The most common mechanism causing blunt carotid injury is hyperextension of the carotid vessels over the lateral articular processes of C1–3 at the base of the skull, which is typically a result of high-speed automobile crashes. There are also scattered case reports of chiropractic manipulation and rapid head turning with exercise causing BCVI. A direct blow to the artery typically occurs in the setting of a misplaced seat belt across the neck during a motor vehicle crash or in the setting of hanging. This injury pattern typically occurs in the proximal internal carotid artery as opposed to the distal aspect. Basilar skull fractures involving the petrous or sphenoid portions of the carotid canal can injure the vessel at this location.
Common mechanisms of injury associated with BCVI include motor vehicle crash (41%–70%), direct cervical blow (10%–20%), automobile versus pedestrian (12%–18%), fall from height (5%–15%), and hanging events (5%). , Most common associated injuries at the time of diagnosis include closed head injuries (50%–65%), facial fractures (60%), cervical spine fractures (50%), and thoracic injuries (40%–51%). ,
Signs and symptoms of BCVI
Case reports, as early as 1967, described BCVI with recognized symptoms of cerebral ischemia, and all patients were symptomatic at the time of diagnosis. Carotid injuries typically are manifested with a contralateral sensory or motor deficit, decreased mental status, or neurologic deficits not explained by closed head injury. A carotid-cavernous fistula may be manifested with orbital pain, proptosis, hyperemia, cerebral swelling, or seizure. Depending on whether the vessel is occluded or whether the resultant injury is a nidus for embolic events, the symptoms may be variable. Patients typically have coexisting traumatic brain injuries that may mask signs and symptoms of BCVI.
Patients may present to the trauma center with obvious signs of BCVI; however, many patients are initially asymptomatic and subsequently develop symptoms after a latent period. Several authors have reported times from 1 hour to several weeks after injury before the development of symptoms. Evaluating an unscreened trauma population, Berne et al. found a median time to diagnosis of 12.5 hours for survivors of BCVI and 19.5 hours for nonsurvivors, suggesting a sufficient window of opportunity for diagnosis and treatment. Neither admission Glasgow Coma Scale score nor baseline neurologic examination correlates with subsequent development of symptoms attributed to BCVI.
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