Trauma, 7th Ed.

CHAPTER 22. Neck

David V. Feliciano and Gary A. Vercruysse


One of the first reported cases of cervical trauma was in Homer’s Iliad when Achilles delivered a fatal lance blow to Hector’s neck, “where the clavicle marks the boundary between the neck and thorax.” This was portrayed by Peter Paul Rubens in about 1631 and hangs in the Museum Boymans-van Beuningen in Rotterdam, the Netherlands.1 Treatment was first described by Ambrose Pare in the mid 16th century when he ligated the right carotid artery and jugular vein of a solider who suffered a bayonet wound. The patient survived, but was aphasic and developed a dense, left-sided hemiplegia.2 The first successful treatment of a major cervical vascular injury did not occur until 1803 when Fleming aboard the HMS Tonnant ligated the common carotid artery of a sailor after a suicide attempt while at sea. The sailor made a prolonged, but complete recovery.3,4 A similar case was reported by Eves of Cheltenham, England, in 1849.5


Knowledge of the surface landmarks of the neck is important for optimal evaluation and management of cervical injuries.6 The defining borders of the neck encompass the area between the lower margin of the mandible and the superior nuchal line of the occipital bone and the suprasternal notch and the upper borders of the clavicles.

Palpable structures from the upper to lower border of the neck include the symphysis menti, which is where the two halves of the body of the mandible unite in the midline. The submental triangle, located between the symphysis menti and the body of the hyoid bone, is bounded anteriorly by the midline of the neck. Laterally, it is bounded by the anterior belly of the digastric muscle, and the mylohyoid muscle forms the floor. The body of the hyoid bone lies opposite the third cervical vertebra. The area between the hyoid bone and the thyroid cartilage is the thyrohyoid membrane, while the notched upper border of the thyroid cartilage is at the level of the fourth cervical vertebra. The cricothyroid ligament or membrane occupies the space between the thyroid cartilage and the cricoid cartilage, which lies at the level of the sixth cervical vertebra and the junction of the pharynx with the esophagus. The interval between the cricoid cartilage and the first tracheal ring is filled by the cricotracheal ligament. Moving inferiorly, the isthmus of the thyroid gland is at the level of the second, third, and fourth tracheal rings. The suprasternal notch can be palpated between the clavicular heads and lies opposite the lower border of the body of the second thoracic vertebra. The sternocleidomastoid muscles, which divide the sides of the neck into anterior and posterior triangles, can be palpated from sternum and clavicle to the mastoid process. The borders of the posterior triangle are the body of the mandible, the sternocleidomastoid muscle anteriorly, and the border of the trapezius muscle posteriorly, along with the clavicle inferiorly.

Posteriorly, the structures of the neck that can be palpated in the midline are the external occipital protuberance, the nuchal groove, and the spinous process of the seventh cervical vertebra (cervical spines 1–6 are covered by the ligamentum nuchae).

The platysma, a thin muscular sheet, is enclosed by the superficial fascia. Its origin is from the deep fascia that covers the upper part of the pectoralis major and deltoid muscles, and it inserts into the lower margin of the body of the mandible. It is the anatomic landmark that is often cited when determining whether a penetrating wound of the neck is superficial or deep. The potential for injury to a vital structure exists when this structure is penetrated.

Beneath the superficial sternocleidomastoid, strap, and trapezius muscles that envelop much of the neck, there are eight body systems that lie within or pass through the neck. Included among these are the following: (1) skeletal system (seventh cervical vertebra, hyoid bone); (2) nervous system (spinal cord and the glossopharyngeal [IX], vagus [X], spinal accessory [XI], and hypoglossal [XII] cranial nerves); (3) respiratory system (oropharynx, larynx, cervical trachea); (4) gastrointestinal system (oropharynx, cervical esophagus); (5) vascular system (common, internal, and external carotid arteries, vertebral arteries, internal and external jugular veins); (6) lymphatic system (thoracic duct); (7) endocrine system (thyroid and parathyroid glands); and (8) immune system (cervical extensions of the thymus).


Penetrating wounds to the neck, particularly those that might involve cervical vascular structures, have been grouped into three separate zones since the original description by Monson et al. in 19697 (Fig. 22-1). A minor modification suggested by Roon and Christensen in 1979 is not of clinical significance.8 Zone I is inferior to the clavicles and manubrium sterni and encompasses all structures in the thoracic outlet. Structures in this zone include the proximal common carotid arteries, vertebral arteries, right and left extrathoracic subclavian arteries, jugulo-subclavian venous junctions, crossover left innominate vein, thoracic duct, trachea, esophagus, spinal cord, proximal brachial plexus, and the vagus nerve. Operative exposure for injuries in Zone I mandates a median sternotomy with cervical extensions, high anterolateral thoracotomy, or a supraclavicular incision with claviculotomy or partial excision of the clavicle, so strong clinical evidence of vascular or visceral injury must be present prior to operation. Zone II is between the thoracic outlet and the angle of the mandible. Structures in this zone include the common carotid arteries and bifurcations, vertebral arteries, internal jugular veins, larynx and cervical trachea, cervical esophagus, spinal cord, and the vagus, spinal accessory, and hypoglossal nerves. Operative exposure for injuries in Zone II mandates an ipsilateral oblique incision along the anterior border of the sternocleidomastoid muscle or a high anterior cervical incision with oblique extensions for possible bilateral injuries. Zone III is between the angle of the mandible and the base of the skull. Structures in this zone include the internal carotid arteries, vertebral arteries, internal jugular veins, pharynx, spinal cord, and the facial, glossopharyngeal, vagus, spinal accessory, and hypoglossal nerves. Operative exposure for injuries in Zone III mandates subluxation of the temporomandibular joint with interdental wiring or vertical ramus mandibulotomy (to be discussed).


FIGURE 22-1 Zones of the neck. (From Monson DO, Saletta JD, Freeark RJ. Carotid vertebral trauma. J Trauma. 1969;9:987. Used with permission.)


Patients with penetrating or blunt trauma to the neck present with overt symptoms and/or signs, moderate or modest symptoms and/or signs, or they are asymptomatic without signs of aerodigestive or vascular injury. The presentation of a patient with overt symptoms or signs will vary depending on the zone of the neck involved. In Zone I a vascular injury from a penetrating wound may cause external hemorrhage from the thoracic outlet or intrapleural exsanguination. A penetrating wound in Zone II or blunt disruption of the cricotracheal junction secondary to a “clothesline” injury may lead to loss of the airway and early asphyxiation. Loss of the airway can occur secondary to the presence of a large hematoma from an injury to the carotid artery, as well. Active hemorrhage from either the carotid artery or internal jugular vein in Zone II can be external and lead to exsanguination or internal bleeding into an associated injury to the trachea, leading to aspiration and asphyxiation. While injures in Zone III are uncommon, exsanguination can occur from an injury to the internal carotid artery at the base of the skull.

Patients with modest or moderate symptoms or signs may present with complaints of hoarseness, dysphagia, or odynophagia and palpable crepitus suggestive of injury to the larynx, trachea, or esophagus. The other presentations in this group are proximity of penetrating wound or blunt contusion to the carotid sheath and/or a stable hematoma suggestive of injury to the carotid artery or internal jugular vein.

An asymptomatic patient will have penetration of the platysma muscle by a gunshot or knife wound or bruising or contusion after blunt trauma, but have no symptoms or signs of injury to the aerodigestive tracts, cervical vessels, the spine, or the spinal cord.

Management of the patient depends on presentation. Overtly symptomatic patients have “A, B, or C” problems on the primary survey as taught in the Advanced Trauma Life Support course, and immediate resuscitation is performed in the emergency center or operating room (see below). Patients with modest or moderate symptoms or signs undergo a diagnostic evaluation referable to the suspected system injured or one that encompasses the aerodigestive and arterial systems. Asymptomatic patients are discharged, admitted for observation, or, in some centers, undergo a limited radiologic evaluation (i.e., cervical computed tomography [CT]).


In patients with exsanguinating external hemorrhage from the thoracic outlet or the lower anterior neck, usually from a penetrating wound, blind finger compression of the bleeding vessel through the skin defect is appropriate in the emergency center (Fig. 22-2). If this is unsuccessful, rapid enlargement of the skin defect with or without local anesthesia is performed. Once again, an attempt is made to compress the bleeding vessel with two or three fingers inserted through the enlarged skin defect. An unsuccessful attempt is followed by tight packing of the area using 3- or 4-in gauze and rapid transport to the operating room. The operative incision will depend on the track of the wound, whether or not manual compression or packing has controlled the bleeding, and the patient’s hemodynamic status. For example, a wound thought to involve the proximal common carotid artery at the base of the neck rather than more proximally in the mediastinum is exposed with the standard anterior oblique invasion on the side of injury. An unstable patient with continuing hemorrhage from the outlet or presumed intrapleural exsanguination should undergo a high anterolateral thoracotomy (fourth intercostal space above the male nipple) on the side of the injury to allow for direct proximal clamping or pack compression of the injured vessel in the thoracic outlet. If the wound is on the right side of the thoracic outlet and the patient is profoundly hypotensive, the sternum is divided transversely and a standard (below the nipple) left anterolateral thoracotomy is performed, as well. This will allow for cross-clamping of the descending thoracic aorta to increase perfusion to the coronary and carotid arteries as resuscitation and vascular repair or ligation are accomplished.


FIGURE 22-2 Algorithm for management of patients with overt symptoms or signs.

In Zone II a penetrating wound may cause impending asphyxiation from a major injury to the trachea (suggested by a continuing air leak from the entrance site). The skin defect is rapidly enlarged with or without local anesthesia, and an endotracheal tube is inserted through the enlarged track following the air bubbles into the distal end of the trachea once it is visualized (Fig. 22-3). The aforementioned “clothesline” injury from blunt trauma may cause cricotracheal separation. Even with impending asphyxiation there should only be one attempt at standard rapid sequence endotracheal intubation.9,10 If this is unsuccessful, a rapid standard tracheostomy is performed between the second and third tracheal rings below the area of injury. Should there be bruising and palpable crepitus over the thyroid cartilage suggestive of an injury to the larynx itself, once again there should only be one attempt at standard endotracheal intubation. Failure to complete this is followed by a rapid standard tracheostomy much as with cricotracheal separation.


FIGURE 22-3 Endotracheal intubation into the distal trachea in a patient with a slash wound to Zone II.

Loss of the airway in Zone II may occur secondary to tracheal deviation or compression from a hematoma resulting from injury to the carotid artery or internal jugular vein, also (Fig. 22-4). With impending asphyxiation, the patient is rapidly moved to the operating room for an attempt at endotracheal intubation over a fiber-optic bronchoscope. If this fails or if the patient is unable to move air when first seen, a cricothyroidotomy is performed rapidly as its high limited central incision (as compared to a standard tracheostomy) avoids the lateral hematoma from the vascular injury.


FIGURE 22-4 Significant Zone II hematoma secondary to gunshot wound of carotid artery. (From Brown MF, Graham JM, Feliciano DV, et al. Carotid artery injuries. Am J Surg. 1982;144: 748–753. Used with permission, © Elsevier.)

With external hemorrhage from a penetrating wound in Zone II, direct compression with a finger or fist on the entrance site is performed in the emergency center and en route to the operating room. The decision on where to make the incision can be made in the operating room after endotracheal intubation has been performed. On rare occasions, there may be internal hemorrhage into the airway when there are adjacent injuries to the carotid artery and trachea. While compression is placed on the carotid artery at the entrance site or at the base of the neck, a cricothyroidotomy is performed. As aspiration is likely to have occurred, fiber-optic bronchoscopy is performed once the injury to the carotid artery has been repaired.

There are two options when exsanguinating hemorrhage occurs from a penetrating wound to the internal carotid artery at the base of the skull in Zone III.11 Finger compression is often only partially successful in this location as the internal carotid artery is deep to the mandible. The quickest option is to maintain manual compression as the patient is moved rapidly to the operating room. Once the patient is intubated and the neck is draped, a #3 or #4 Fogarty balloon catheter is inserted into the wound, advanced 2 cm, and the balloon is inflated12,13 (Fig. 22-5). If hemorrhage continues, the balloon is deflated and advanced 1 cm at a time and inflated till balloon tamponade controls the hemorrhage. The catheter is then sutured to the skin and the balloon left inflated for 24 hours. When external passage of the balloon catheter is partially successful or unsuccessful, a Foley balloon catheter is passed as it has a larger balloon. If this is unsuccessful, as well, the catheter is removed and manual compression is applied once again. A standard oblique cervical incision on the anterior border of the sternocleidomastoid muscle is made, the internal carotid artery is exposed, and a small arteriotomy is made in the middle of a 6-0 polypropylene purse-string suture. Once again, a #3 or #4 Fogarty balloon catheter is passed through the arteriotomy and inflated sequentially until balloon tamponade is successful. On rare occasions, it may be necessary to pass balloon catheters through the entrance site and through the internal carotid artery simultaneously. A baseline EEG is performed at this time. This is followed by a contralateral carotid arteriogram to evaluate the extent of crossover flow to the side of the brain that has been rendered possibly ischemic by balloon occlusion of the internal carotid artery. Even in the patient with adequate crossover flow, every attempt should be made to keep the patient normotensive with a 100% oxygen saturation level. An intracranial pressure monitor is appropriate, as well, so that treatment can be initiated when ischemic edema occurs. When the baseline EEG is abnormal and the contralateral carotid arteriogram documents inadequate crossover flow, cerebral ischemia is occurring. This is expected in patients who have had a period of significant hypotension secondary to exsanguination prior to inflation of the balloon. In the past, it was recommended that a patient with ipsilateral cerebral ischemia undergo a saphenous vein bypass from the cervical internal carotid artery to the petrous portion through a small temporal craniotomy.14 Currently, deflation of the balloon(s) and rapid insertion of an endovascular stent into the high internal carotid artery would be the procedure of choice.15,16


FIGURE 22-5 A Fogarty balloon catheter was inserted into a high cervical stab wound to control exsanguinating hemorrhage. Deflation of the balloon and removal of the catheter were performed on the fourth day after insertion. (From Feliciano DV. Management of penetrating injuries to carotid artery. World J Surg. 2001;25:1028–1035. Used with permission.)


image Zone I

Hemodynamically stable patients with penetrating wounds in proximity to the thoracic outlet should undergo surgeon-performed ultrasound and a chest x-ray. The ultrasound will rule out an associated cardiac injury and document the presence of a hemothorax or pneumothorax. The chest x-ray will aid in tracking the course of the missile and in documenting the presence of a hematoma in the superior mediastinum, base of the neck, or supraclavicular area. There have been several retrospective studies that have documented that a normal physical examination and chest x-ray virtually exclude a vascular injury at the thoracic outlet.17,18 Even so, certain trauma centers will use a screening CT as an added study to determine the track of a penetrating wound in this area.19 When the track of a missile or knife wound is in proximity to vessels at the thoracic outlet and there is an adjacent hematoma on the chest x-ray, digital subtraction arteriography (DSA) of the carotid, vertebral, and subclavian arteries or a CT arteriogram (CTA) is performed. This will document the presence and location of a vascular injury and allow for the choice of an appropriate operative incision.


FIGURE 22-6 Evaluation of patients with modest or moderate symptoms or signs or an asymptomatic patient.

There are symptoms (hoarseness, dysphagia, odynophagia), signs (palpable crepitus, continuing air leak through the wound), or findings on a cervical or chest x-ray (cervical or mediastinal air) that suggest a possible injury to the trachea or esophagus. The diagnostic workup is described in Section “Zone II.”

image Zone II

The approach to possible injuries in this zone has varied considerably over the past 55 years. Based on the report by Fogelman and Stewart20 at Parkland Memorial Hospital in 1956, mandatory exploration for wounds penetrating the platysma muscle was recommended. This recommendation was based on a mortality rate of 6% in patients undergoing early operation versus 35% in those undergoing delayed operation.

It quickly became obvious, however, that cervical explorations in all patients (overtly symptomatic, modestly or moderately symptomatic, asymptomatic) with penetration of the platysma muscle in Zone II resulted in a “negative” exploration rate of approximately 50%.21 A more selective approach to operation based on symptoms and signs as described above was then adopted by many centers. One review article in 1991 comparing the two approaches noted that mandatory cervical exploration for platysma penetration had a mortality rate of 5.8% versus 3.7% for a selective approach.22 Of interest, a negative or nontherapeutic cervical operation occurred in 46.2% of patients treated with mandatory exploration. When patients with modest or moderate symptoms or signs or those who are asymptomatic are managed with a selective approach, only 55–65% eventually come to operation. Numerous large studies subsequently verified the safety of a selective approach in the 1980s and 1990s.2333

Physical Examination

Physical examination alone is highly accurate in evaluating an asymptomatic patient with a penetrating (through the platysma muscle) stab wound in Zone II. This is true for patients with gunshot wounds in Zone II, as well, as long as the track is tangential or away from the vascular (lateral) or aerodigestive tract (central).3335 With platysma penetration, but without further evaluation by CT, CT angiography, duplex ultrasonography, or endoscopy, serial examinations of the patient’s neck every 6–8 hours for 24–36 hours are appropriate.

Computed Tomography

CT has been used as an adjunct to physical examination over the past decade in selected centers.19,36,37 In asymptomatic patients with a normal physical examination after a penetrating wound in Zone II, it “contributes minimally” to the sensitivity of physical examination.37 When patients have no “hard signs” of vascular injury in Zone II, but are “at risk for injury to vital structures within the neck,” CT can demonstrate a trajectory away from these structures.19With such a trajectomy, “invasive studies can often be eliminated from the diagnostic algorithm.”19 A more recent study using multislice helical computed tomography/angiography (MCTA) documented a “100% sensitivity and 95.5% specificity in detecting all vascular and aerodigestive injuries sustained.”38

Arteriography, Duplex Ultrasonography, Color Flow Doppler, CTA

Patients with “hard” signs of a vascular injury in Zone II present with external bleeding, bleeding into the trachea or esophagus, an expanding or stable large hematoma, and/or an audible bruit/palpable thrill. Patients with bleeding or an expanding or large stable hematoma undergo an emergency cervical exploration. A patient with a likely arteriovenous fistula should have some type of vascular diagnostic study performed. Should a fistula between the internal carotid artery and jugular vein be present, an endovascular stent rather than cervical exploration may be chosen.

In patients with “soft” signs (modest or moderate signs) of a vascular injury in Zone II such as a history of bleeding at the scene, proximity of a stab, missile, or pellet track, or a small nonexpanding hematoma, the role of arterial diagnostic studies remains controversial. As noted above, physical examination alone is highly accurate in ruling out an arterial injury in the asymptomatic patient. Much as in evaluating possible peripheral arterial injuries, however, there is at least a 3–5% chance of a surgically reparable arterial lesion in a patient who presents with a cervical vascular “soft sign.” And it is likely that a combination of “soft signs” (i.e., proximity of wound and small hematoma) will increase the need for surgical intervention. Therefore, some type of diagnostic study is performed in patients with “soft signs” in most centers (Fig. 22-7).


FIGURE 22-7 Pellet wound in an asymptomatic patient caused 30% transection of left common carotid artery in Zone II. Arteriogram performed secondary to traverse of missile through Zone II.

Four-vessel cerebral arteriography was the longtime standard of care for evaluating the carotid and vertebral arteries. The technique is highly accurate in diagnosing arterial injuries, eliminating nontherapeutic explorations, and allowing for transcatheter embolization when indicated.39,40 The disadvantages include the time required to allow the interventional radiology team to return to the hospital at night, the dye load required, and the low yield when all asymptomatic or modestly symptomatic patients are studied.41

Duplex ultrasonography, a combination of real-time brightness (B)–mode imaging and pulsed Doppler velocimetry, has been used in the diagnosis of atherosclerotic occlusive decrease of the carotid artery for 35 years.4143 Basically, the technology produces images that define anatomy and a spectral profile that documents flow through the vessel. Numerous reports during the 1990s documented the ease and accuracy of the technique when applied to patients with penetrating wounds in Zone II.4447 It was suggested that duplex replace conventional arteriography because of ease of performance and the significant cost-savings that would result.4648 This did not happen over time in most trauma centers as the technique can be performed only by a registered vascular technologist or experienced vascular surgeon trained in duplex.

A related technique of “color flow Doppler” has been used to evaluate the carotid arteries after penetrating trauma to Zone II, as well.49,50 In this technique, flow to and from the point of the Doppler examination is represented on a color scale. Several studies in the 1990s documented that the combination of a careful physical examination and color flow Doppler was a safe alternative to routine contrast angiography.49,50

For the past 15 years there have been ongoing studies to determine the accuracy of CTA, particularly in patients with possible blunt cerebrovascular injuries (BCVI; to be discussed). Penetrating cervical injuries have been studied, as well, with early reports coming from the Hospital Universitario San Vicente de Paul in Medellin, Colombia.51,52 Based on the ease and speed of obtaining accurate images reconstructed at 1-mm intervals, the authors from this well-known trauma center concluded that “helical CT can replace conventional angiography in this setting” (penetrating injuries to the neck).52 Another early report from 2005, before the current generation of 32- and 64-slice detectors, documented that the use of CTA significantly decreased the number of conventional arteriograms required and negative cervical explorations performed.53 The enthusiasm for using CTA is tempered, of course, by continuing concerns about its accuracy in evaluating possible BCVI.54 But the aforementioned 2006 study with a 100% sensitivity in evaluating patients with penetrating cervical wounds is certainly reassuring.38 Based on available data, it appears that multidetector helical CTA is slowly replacing conventional arteriography as a rapid screening modality to evaluate possible arterial injuries in Zone II after penetrating trauma. An equivocal screening study or one in which the anatomic area of interest is obscured by artifacts created by adjacent metallic fragments should be followed by a conventional arteriogram.


Patients with modest or moderate symptoms of an esophageal injury present with complaints of deep cervical pain, dysphagia, odynophagia, or hematemesis. On examination, palpable crepitus and deep cervical tenderness may be present. An x-ray of the neck will usually demonstrate retropharyngeal or retroesophageal air in the soft tissues, while a pneumomediastinum will be present on a chest x-ray if there has been a delay in the patient’s arrival in the trauma center.

Historically, the time-honored “sip test” was performed in such patients in centers with limited resources.30 A patient who was able to swallow a mouthful of water without severe discomfort was felt to have only a small injury or no injury of the cervical esophagus and was admitted for observation only. The patient who had severe pain with swallowing would then undergo standard diagnostic testing to evaluate for the presence of an esophageal injury.

While CT has now been widely applied in the diagnostic evaluation of patients with penetrating and blunt cervical trauma as previously noted, its accuracy in detecting an injury of the cervical esophagus is unclear. This is because several of the reports in which CT has been evaluated do not include any patients with esophageal injuries.36,38 For this reason, asymptomatic patients with air in the soft tissues of the neck after trauma, those with a positive “sip” test, or those with a combination of modest/moderate symptoms and signs of an esophageal injury undergo the standard diagnostic evaluation using a contrast esophagogram and endoscopy.5557

While there is a risk of secondary necrotizing pneumonitis and pulmonary edema if the contrast agent Gastrografin (meglumine sodium) is aspirated, it remains the initial contrast agent of choice for esophagograms in most centers.56The accuracy of detecting an injury to the cervical esophagus with this agent is 57–80%.5760 A “thin” barium study follows a negative Gastrografin swallow or has been used as the primary contrast agent in some centers.56,57

As contrast esophagograms with either Gastrografin or thin barium have a less than 100% sensitivity in diagnosis, flexible esophagoscopy is next performed in the at-risk patient with a negative contrast study. It has long been known that the combination of a contrast study and esophagoscopy has an accuracy of nearly 100% in patients with esophageal injuries in Zone II.61 In two studies describing the results of flexible esophagoscopy specifically over the past 16 years, sensitivity was 98.5–100%, specificity 96–100%, and accuracy 97–99.3%.62,63

Laryngoscopy/Fiber-Optic Bronchoscopy/CT

Patients with modest or moderate symptoms of an injury to the larynx or cervical trachea present with hoarseness, stridor, or hemoptysis. On examination, contusions over the larynx or cervical trachea, palpable crepitus, deep cervical tenderness and bubbling, or an ongoing leak of air from a penetrating wound may be present. As with injuries of the cervical esophagus, paratracheal air or a pneumomediastinum will usually be present on cervical and chest x-rays.

In asymptomatic patients with air in the soft tissues of the neck or those with a combination of modest/moderate symptoms and signs of a tracheal injury, the traditional diagnostic evaluation includes laryngoscopy and fiber-optic tracheoscopy and bronchoscopy. Laryngoscopy will diagnose and localize an injury to the supraglottic, glottic, or subglottic larynx.6 A vertical fracture of the thyroid cartilage with rupture of the thyroepiglottic ligament is an example of a supraglottic injury and results in retraction of the epiglottis. A fracture of the thyroid cartilage with an associated rupture of the thyroarytenoid muscles extending into the true vocal cords and aryepiglottic folds is an example of a glottic injury and results in hoarseness or stridor. As previously described, a significant injury to the lower thyroid cartilage and cricoid cartilage with separation from the trachea would result in acute respiratory distress long before a laryngoscopy could be performed.64

Fiber-optic tracheoscopy and bronchoscopy is used to evaluate stable patients with suspected injuries to the trachea and major bronchi.65,66 The technique allows for placement of an endotracheal tube over the fiber-optic bronchoscope in patients with impending airway distress and for detection of penetrating or blunt perforations.

Of interest, the aforementioned study using multidetector CT (MCT) in penetrating wounds of the neck documented the presence of 6 tracheal injuries in the 12 patients with positive MCT studies.38 Larger studies will be necessary to confirm the diagnostic accuracy of MCT in detecting laryngeal and tracheal injuries.

image Zone III

Historically, conventional arteriography was recommended for all stable patients with penetrating wounds in Zone III.67 Much as with mandatory diagnostic studies and/or operation in all patients with penetrating wounds of the neck, the approach to wounds in Zone III is now more selective.68 As with the other zones of the neck, patients with hard signs of an arterial injury in Zone III have a greater than 90% chance of having a positive cervical exploration. Patients without hard signs, however, rarely have an arterial injury on conventional arteriography that will require surgical intervention.6870 Of course, arteriography or CTA will be of value in a select number of stable patients with hard signs not including bleeding or a combination of soft signs such as a history of bleeding, proximity of wound, and/or a nonexpanding hematoma in this location. When a limited arterial injury is diagnosed on one of these studies, observation or endovascular therapy would be appropriate (to be discussed).


While BCVI were first described in 1872, knowledge about pathophysiology, screening, diagnosis, and treatment has mainly accumulated over the past 30 years.7174

The unique relationship of the carotid and vertebral arteries and the skull and cervical vertebrae is a causative factor for these injuries. The common carotid artery bifurcates into the internal and external carotid arteries at the level of the fourth cervical vertebra. The internal carotid artery passes upward and is then fixated in the carotid canal of the petrous portion of the temporal bone until it reaches the foramen lacerum. Most blunt injuries occur in the internal carotid artery below this fixed area in the skull. In a similar fashion, the second portion of the vertebral artery passes through the transverse foramina (foramina transversaria) of the cervical vertebrae C2–C6 before curving behind the lateral mass of the atlas.

The mechanism of blunt injury to the internal carotid artery can be a direct cervical blow, a basilar skull fracture involving the carotid canal, or a fracture of the petrous portion of the temporal bone. Most authors, however, feel that the most common mechanism is a cervical hyperflexion/hyperextension injury with stretching of the vessel over the bodies of cervical vertebrae C1–C3.75 The hyperflexion/hyperextension injury is a presumed sequela of the use of shoulder harness restraints in the modern car. Prior to the use of these, many front-seat victims of head-on motor vehicle crashes sustained hyperextension injuries only on impact with the windshield. The hyperflexion–hyperextension injury to the internal carotid artery may be compounded by lateral rotation of the neck away from the side of the shoulder restraint.75,76

The mechanism of blunt injury to the vertebral artery may be a fracture of one of the foramina transversaria or a subluxation-type injury in the cervical spine with a locked facet, destroyed facet, or dislocation with instability. Depending on the cause, direct trauma to the vertebral artery (i.e., a fracture) or distraction of the foramina with secondary stretching of the artery (i.e., dislocated facet) will result.

image Incidence/Screening

As the recent incidence of BCVI is only 0.58–1.03% of all admissions for blunt trauma, there has been long-term interest in developing and analyzing screening criteria to increase the yield of diagnostic studies.7783 There is, however, no current consensus on which risk factors mandate screening for BCVI. The group at Denver Health Medical Center, University of Colorado, has described liberal screening criteria that include symptoms/signs of BCVI and associated injuries from a “high-energy” mechanism80 (Table 22-1). A more discrete list of criteria from the University of Tennessee Health Science Center, Memphis, includes the following: (1) neurological exam not explained by brain imaging; (2) skull base fractures involving the foramen lacerum; (3) Horner’s syndrome; (4) LeFort II or III facial fractures; (5) cervical spine fracture; and (6) soft tissue injury in the neck (e.g., seatbelt injury or hanging).54,79,84 Using these criteria for screening documented an overall incidence of BCVI of 0.58% and an incidence of BCVI in the screened patients (748/20,049 = 3.7%) of 16%.54 In another recent study using similar criteria in 9,935 patients from the East Texas Medical Center in Tyler, the incidence of a carotid artery BCVI was 0.43% and vertebral artery BCVI was 0.59%.82

TABLE 22-1 Screening Criteria for BCVI


When evaluating the yield of individual criteria, the Memphis group noted that the incidence of BCVI when only one criterion was present ranged from 6% to 17%.54 When similar criteria were analyzed at the University of Cincinnati in 2009, the respective incidences of BCVI varied widely. For example, skull base fractures through or near the carotid canal had a BCVI incidence of 16.9%, midface fracture or fracture dislocation of the cervical spine had an incidence of 38.8/30.7%, and Raeder or Horner’s syndrome had an incidence of 80%.81 Of interest, a recent report based on an analysis of 1,398,310 patients with blunt trauma in the National Trauma Data Bank of the American College of Surgeons (BCVI incidence = 0.15%) noted that BCVI was “poorly predicted by modeling with other injuries.”83

image Imaging for Screening

With the availability of CTA over the past decade, there has been increasing enthusiasm for using this modality rather than digital subtraction cerebral arteriography to screen for BCVI.

There have been numerous studies suggesting that 16-slice multidetector CTA is a very accurate modality when screening for BCVI. In one study by Berne et al.85 in which four-vessel cerebral arteriography was performed if a 16-slice CTA was positive or equivocal for BCVI, no patient with a negative CTA subsequently developed neurological symptoms. Eastman et al.86 described 146 patients who had both a 16-slice CTA and cerebral arteriography and noted a 97.7% sensitivity, 100% specificity, and 99.3% accuracy for CTA. In the study by Biffl et al.87 in which 331 patients had a 16-slice CTA and abnormal studies were followed by a conventional arteriogram, no patient with a negative CTA developed a BCVI.

Much as with the lack of consensus regarding screening criteria, there are numerous studies that question the accuracy of CTA in detecting BCVI. Goodwin et al.88 performed CTA with a 16- or 64-slice scanner followed by conventional angiography 24–48 hours later in 158 patients. The combined results of CTA with 16- or 64-slice scanner were sensitivity and specificity of 97% and 41%, respectively. Similar unacceptable sensitivities have been noted in other recent studies, as well.89,90 Also, only a limited number of patients with possible BCVI have been studied with magnetic resonance angiography at this time.91 Therefore, this study cannot be recommended.

image Types of Injuries

Most centers use the blunt carotid arterial injury grading scale developed at Denver Health Medical Center by Biffl et al. in 1999.92 This grading scale is described as follows: Grade I, luminal irregularity or dissection with a 25% narrowing; Grade II, dissection or intraluminal hematoma with ≥ 25% luminal narrowing, intraluminal thrombus, or raised intimal flap; Grade III, pseudoaneurysm; Grade IV, occlusion; and Grade V, transection with free extravasation.

image Management

Only observation without the administration of anticoagulants is appropriate temporarily in patients with a Grade I–IV injury and an associated traumatic brain injury or solid organ injury. The timing of initiation of anticoagulant therapy in the described patient groups is unclear at this time. It should, however, be based on the presence or absence of neurological findings, the magnitude of the BCVI, and the magnitude of the associated injuries. The use of anticoagulants in this situation is somewhat analogous to the use of the same for prophylaxis against deep venous thrombosis in patients with traumatic brain injuries. In one recent study using early enoxaparin in selected patients with traumatic brain injuries, but without CT exclusion criteria, the safety of this approach was demonstrated.93

Early heparinization with a continuous dosage of 10 U/(kg h) of heparin to a target partial thromboplastin time of 40–50 seconds is appropriate for patients with BCVI Grade I–IV injuries.84,94 If necessary, antiplatelet therapy may be substituted when heparin is contraindicated.95 Depending on the rate of hemorrhage, a Grade V injury is treated with surgery after subluxation of the temporomandibular joint with interdental wiring or vertical ramus osteotomy as previously noted or insertion of an endovascular stent with insertion of extraluminal coils as needed.

The early enthusiasm for endovascular stenting for primarily Grade III injuries92,9699 was tempered somewhat by the follow-up report from the Denver group in 2005 in which carotid stents had an occlusion rate of 45%.100Subsequent reports, however, have demonstrated a much lower occlusion rate.101104 In Memphis, a patient with a blunt dissection (Grade I or II) or traumatic aneurysm (Grade III) on the original CTA or conventional arteriogram is placed on anticoagulants for 1–2 weeks. Three days prior to a repeat imaging study, the patient is placed on aspirin and clopidogrel bisulfate. Should the repeat imaging study document progression of the dissection or worsening of the traumatic aneurysm, an endovascular stent is placed. Persistence of a traumatic false aneurysm outside the stent is followed by placement of a coil through the stent. The patient then continues on long-term aspirin and clopidogrel bisulfate (Timothy C. Fabian, MD, personal communication).

When endovascular and operative therapies were compared in 842 patients with blunt injuries of the carotid arteries in the National Trauma Data Bank, there was no functional or survival advantage for either group.105


image General Principles/Incisions

Once an airway has been established using the emergency techniques previously described or with standard endotracheal intubation, a rolled sheet is placed transversely under the shoulders to hyperextend the neck. The patient is then placed in a sitting position to bring the operative field closer to the surgical team.

With a unilateral track of penetrating wound or with any aerodigestive injury below the larynx in Zone II, an ipsilateral oblique incision is made along the anterior border of the sternocleidomastoid muscle. The length depends on the location of the known or presumed injury, the likelihood of a significant vascular injury, and the experience of the surgeon. For example, a patient with a large unilateral hematoma in Zone II overlying a presumed injury to the carotid artery or internal jugular vein should have an incision extending from the sternum inferiorly to the mastoid process superiorly. Such an extensive incision will allow for proximal and distal vascular control around the injury before entering the hematoma. In contrast, a patient without symptoms and signs of a vascular injury despite a deep stab wound in Zone II may be explored through a more limited oblique incision by an experienced surgeon.

When the track of a missile is through Zone II bilaterally, a high anterior collar incision at the level of the track is appropriate. Depending on the patient’s hemodynamic status, superior and inferior subplatysma flaps are raised before the midline raphe of the sternohyoid muscles is opened longitudinally or the sternohyoid muscles are separated from the sternocleidomastoid muscles laterally. An injury on either side of the neck that is higher than expected can be exposed through an oblique extension of one side of the collar incision.

The appropriate incision for probable or documented injury in Zone I will depend on the likely injury, the patient’s hemodynamic status, and the experience of the surgeon. A profoundly hypotensive patient with active intrapleural hemorrhage from an injury to a great vessel in the superior mediastinum or a subclavian vessel behind the clavicle should have an ipsilateral high (above the nipple) anterolateral thoracotomy. If the injury is on the right side, a trans-sternal extension and left anterolateral thoracotomy (above or below the nipple) is added to allow for cross-clamping of the descending thoracic aorta as part of resuscitation. Vascular control is then obtained with pack compression or direct clamping. When the patient is modestly hypotensive (systolic blood pressure 90–120 mm Hg) and there is a hematoma in the superior mediastinum, a median sternotomy with a cervical or supraclavicular extension is appropriate. In the stable patient with a localized vascular injury on a CTA or conventional arteriogram, a median sternotomy or supraclavicular incision is chosen depending on which vessel is injured.

In the rare patient with hemorrhage from a penetrating wound to the internal carotid artery at the base of the skull in Zone III, a balloon catheter is passed through the entrance site as previously noted. Inadequate vascular control with the balloon inflated should prompt an ipsilateral oblique cervical incision to allow for exposure of the internal carotid artery and transarterial passage of a Fogarty balloon catheter for internal tamponade.106

image Injury to the Carotid Artery

Patients with “hard” signs of an arterial injury such as external hemorrhage from Zone II, internal hemorrhage into the trachea or esophagus, or the presence of a pulsating/expanding hematoma in the anterior triangle of the neck should undergo immediate cervical exploration. In patients with loss of the carotid pulse, but no neurological deficit, many centers choose to perform a CTA or conventional arteriogram to verify thrombosis of the internal carotid artery. Management of a documented thrombosis from a penetrating wound in the asymptomatic patient (observation vs. revascularization) is controversial. The presence of a suspected carotid artery–internal jugular vein fistula, particularly in high Zone II or in Zone III, should prompt a CTA or conventional arteriogram, as well. Depending on local expertise, a documented arteriovenous fistula may be treated with an endovascular stent or an open repair.

As previously noted, patients with “soft” signs of an arterial injury still undergo a diagnostic workup in many centers. Included would be patients with a history of bleeding at the scene or in transit, a gunshot wound passing through Zone II, a stable hematoma, or a neurological deficit such as hoarseness from an injury to the vagus nerve proximal to the origin of the recurrent laryngeal nerve. Management will vary depending on the magnitude of any injury to the carotid artery documented on a CTA, conventional arteriogram, duplex ultrasonography, or color flow Doppler examination. In general, extravasation, the presence of an early, pulsatile pseudoaneurysm, significant disruption of the intima, or significant disruption of flow to the brain mandates ipsilateral cervical exploration and repair of the common or internal carotid artery.

Patient with an Associated Neurological Deficit

A neurological deficit in a patient with a penetrating wound to the common or internal carotid artery may be due to cerebral ischemia from the injury itself, hypotension from hemorrhage, acute alcoholic intoxication, or the use of illicit drugs. In patients with any neurological deficit short of coma (GCS ≤ 8), immediate repair of the carotid artery is indicated as the etiology of the deficit may be unknown.106112The often-quoted review article by Liekweg and Greenfield in 1978 documented that a “favorable outcome” occurred in only 27% of patients undergoing carotid revascularization versus 25% undergoing ligation when “coma” was the presentation.106

Exposure of Zone III Injuries

When stenting is not appropriate for an injury to the internal carotid artery in Zone III (i.e., active hemorrhage, pseudoaneurysm has failed stenting with trans-stent coil, internal carotid artery very small), an operative approach is indicated. Exposure of the distal internal carotid artery at the base of the skull is obtained by a “stepladder” mandibulotomy,113 subluxation of the temporomandibular joint with interdental wiring114116 or with monocortical screws and steel wiring,117 or a vertical ramus osteotomy.118


In the absence of other significant injuries, systematic heparinization (100 U/kg) is used when any repair more complex than lateral arteriorrhaphy is needed (Table 22-2). Repairs of the carotid artery are accomplished using standard techniques including the following: (1) minimal debridement and lateral arteriorrhaphy with interrupted 6-0 polypropylene sutures for a lateral defect; (2) patch angioplasty with saphenous vein, thin-walled polytetrafluoroethylene, or bovine pericardium for loss of one wall; (3) segmental resection and end-to-end anastomosis for through-and-through injuries or segmental disruption; and (4) segmental resection and insertion of a saphenous vein or polytetrafluoroethylene interposition graft.11,108,110 On rare occasions, an injury to the proximal internal carotid artery may be repaired by ligating and dividing the distal external carotid artery and using the proximal segment as a transposition graft.

TABLE 22-2 Principles of Repair of the Carotid Artery


In a young patient with excellent back-bleeding from the internal carotid or common carotid artery after distal vascular control has been attained, an intraluminal shunt is not indicated as the repair is completed. With a rare distal injury in the internal carotid artery in upper Zone II or in Zone III, insertion of a graft may take longer than 30 minutes. In this situation, a temporary intraluminal shunt should be considered as the repair is completed.

As cross-clamping of the common or internal carotid artery after a period of hypotension and during a period of repair may result in ipsilateral cerebral ischemia, postoperative care is critical.119 The possibility of an ischemia–reperfusion injury with secondary ipsilateral cerebral edema mandates avoiding hypotension and hypoxemia as well as performing serial careful postoperative neurological examinations.

Should the patient have no improvement of preoperative neurological symptoms or develops neurological deterioration in the early postoperative period, an emergency CT of the brain is performed. Ipsilateral cerebral edema is treated with the insertion of an intracranial pressure monitor as well as standard drainage and medications such as mannitol.

In one older series, the survival rate for all 129 patients undergoing operation on an injured carotid artery was 75%.108 When patients failing resuscitation were excluded, the survival rate was 85%.108

Injury to the Vertebral Artery

An injury to the vertebral artery such as dissection from blunt trauma or intimal disruption, a pseudoaneurysm, arteriovenous fistula, or active hemorrhage from a penetrating wound is usually diagnosed on a CTA or other imaging study in the hemodynamically stable patient. Appropriate treatment is the placement of an endovascular stent for a pseudoaneurysm or intimal lesion and acute balloon occlusion, if needed, followed by coil embolization of an arteriovenous fistula or active hemorrhage.120,121

In patients undergoing a cervical exploration for hemorrhage or a suspected injury to the aerodigestive systems, active hemorrhage originating from the posterolateral neck adjacent to the spinal transverse processes is likely from an injured vertebral artery. While detailed descriptions of operative approaches to the different levels of the vertebral artery are available, they are almost never utilized in the modern era.122124 As proximal ligation of the ipsilateral vertebral artery originating from the second portion of the subclavian artery is unlikely to stop the hemorrhage, packing with bone wax or gauze is commonly utilized and is always successful. Many surgeons leave the bone wax in place, while the gauze pack will need to be removed at a reoperation.

With occlusion of the vertebral artery by the trauma itself or by operative ligation or coil embolization, antegrade thrombosis is a risk in the postoperative/postprocedure period. For this reason, anticoagulation with heparin is appropriate before discharge. Whether long-term anticoagulation is necessary is unclear.

When unilateral vertebral artery ligation, packing, or coil occlusion is performed, a mortality of 5–15% expected.122,125 Deaths are invariably due to prehospital exsanguination or an associated injury to the brain.

image Injury to the Internal Jugular Vein

Lateral venorrhaphy is appropriate for wall defects, while more extensive injuries are treated with ligation. As bilateral ligation of the internal jugular veins may result in pseudotumor cerebri, every effort should be made to repair one internal jugular vein when bilateral injuries are present.

image Injury to the Esophagus

The simplest technique to expose the cervical esophagus is to dissect down to the cervical vertebral bodies and then lift the posterior wall of the esophagus off them by stripping with a finger (Table 22-3). Exposure of the anterior esophagus requires some care, as the recurrent laryngeal nerves are located in the tracheoesophageal groove at the lower cervical level. Once the esophagus has been dissected circumferentially, it can be looped with a finger or Penrose drain and carefully inspected by pulling it toward the operating surgeon. Any area of hematoma staining should be gently explored with a scissor to see if the mucosa underneath has been perforated. If the mucosa is intact, the esophageal muscle is reapproximated with several simple interrupted sutures of 3-0 absorbable material.

TABLE 22-3 Principles of Repair of the Esophagus


On occasion, it may be necessary to have the anesthesiologist help make the diagnosis of a small occult perforation in the cervical esophagus. One technique is to compress the distal esophagus at the thoracic inlet and to fill the proximal esophagus with 30–50 mL of methylene blue dye in saline (one ampule in 200 mL). Full-thickness staining of dye at any location suggests that a perforation is present. Another technique is to place the tip of a nasogastric tube in the midcervical esophagus, compress the distal esophagus with a finger or noncrushing clamp, and have the anesthesiologist inject 30–50 mL of air into the proximal esophagus through the nasogastric tube. By filling the operative field with saline solution, any air leak from an occult perforation would be seen as bubbling into the saline.

With a limited injury from a stab or gunshot wound, minimal debridement is performed. A two-layer repair starts with a continuous 3-0 absorbable suture closure of the mucosa, preferably in a transverse direction. The repair is completed by placing interrupted 3-0 absorbable sutures through the muscularis layer of the esophagus. As there is a 5–25% leak from repairs of the cervical esophagus historically, a small Penrose drain or closed suction drain is placed adjacent to the repair before closure of the incision.126129 This drain is brought anteriorly so as not to cause erosion of the carotid artery laterally.

When there has been a loss of tissue from one wall or the diagnosis of a perforated cervical esophagus has been delayed, a simple lateral suture repair or end-to-end anastomosis is not appropriate. A lateral blowhole esophagostomy at the site of the defect is placed over a red Robinson catheter (like a rod under a loop colostomy) located in the incision or lateral to it.130,131 Whether a tie of absorbable suture material should be placed around the distal side of the elevated loop remains controversial.131,132 Keeping the esophagus in continuity, even with a large defect, will avoid the need for a colon interposition or free jejunal graft in the future. Conversion to a loop esophagostomy rather than performing a tenuous repair avoids the complication of a large esophagocutaneous fistula with secondary problems such as tracheoesophageal fistula, carotid artery blowout, or wound infection in the postoperative period. The esophagostomy has a tendency to shrink and to pull to the posterior midline over time, and delayed closure is often much easier than expected (Fig. 22-8).


FIGURE 22-8 Closure of loop cervical esophagostomy was a relatively easy procedure in this patient who had esophagogastrectomy after a distal esophageal repair leaked.

image Injury to the Trachea

Anterior or lateral perforations are not debrided and are closed with interrupted full-thickness 3-0 absorbable sutures to create an airtight seal (Table 22-4).66,132 When there is tissue loss in the anterior or lateral trachea, a tracheostomy tube can be placed into the defect until a decision is reached on use of a vascularized muscle patch or formal reconstruction. Should the large defect be in the proximal trachea, the sternal head of the sternocleidomastoid muscle is detached, rotated medially, and sewn directly to the defect to create an airtight seal after removal of the tracheostomy tube. Resection of a large defect, mobilization of both ends of the trachea, and an end-to-end anastomosis have never been performed at a first operation in the senior author’s experience.

TABLE 22-4 Principles of Repair of the Trachea


When there is a large defect in the membranous portion of the cervical trachea, a three-sided longitudinal anterior pericardial flap based superiorly is created after a median sternotomy is performed. The pericardial flap is then sewn to the defect in the membranous trachea to create an airtight seal.

Late reconstruction of a previously injured trachea with a segmental partial loss of tissue is best performed by a thoracic surgeon with experience in tracheal resection and reconstruction. Dissection should be limited at the 3 and 9 o’clock areas of the trachea to avoid devascularizing the ends. Both laryngeal lowering and bilateral lung elevating procedures may be necessary with gaps in the trachea exceeding 5–6 cm.133 Repair is accomplished with interrupted 3-0 absorbable sutures, no protective tracheostomy is performed, and a sternocleidomastoid muscle flap may be used to buttress the suture line (see below).

image Combined Injuries to the Trachea–Esophagus, Trachea–Carotid Artery, or Esophagus–Carotid Artery

A postoperative complication rate of 74% was reported in one older series of 23 combined tracheoesophageal injuries.134 Analysis of the complications documented that the majority were due to leaks from the esophageal repair. This led to wound infections, tracheoesophageal fistulas, secondary pneumonias, and blowouts of adjacent repairs of the carotid artery. With adjacent repairs of the trachea and esophagus, trachea and carotid artery, or esophagus and carotid artery, a vascularized sternocleidomastoid muscle flap should be wrapped around the visceral repair135 (Fig. 22-9). This should lower the incidence of a leak from the visceral repair and, if a leak occurs, protect the adjacent arterial repair.


FIGURE 22-9 The sternal head of the left sternocleidomastoid muscle was interposed between tracheal and esophageal repairs after a gunshot wound in Zone II.

The sternocleidomastoid muscle has a tripartite blood supply that includes the thyrocervical trunk, superior thyroid artery, and occipital artery. Therefore, it can be detached from the sternum and clavicle inferiorly or the mastoid process superiorly and rotated to cover the repair of the trachea or esophagus and act as a vascularized buttress. With combined injuries of the trachea, esophagus, and/or carotid artery at the upper or mid-area of Zone II, the first step is detaching the sternal head of the sternocleidomastoid muscle from the sternum if the muscle is bulky. If it is not, both the sternal and clavicular attachments are divided. Either the detached sternal end or the entire muscle is then mobilized and rotated medially to buttress the tracheal or esophageal repair and separate it from the repair in the carotid artery. The mobilized muscle is sewn in place with multiple interrupted sutures of 3-0 absorbable material. Any esophageal repair is drained anteriorly with the drain and drain track away from the repair in the carotid artery.


Patients with penetrating or blunt injuries to the three zones of the neck present with overt symptoms or signs, moderate or modest symptoms or signs, or they are asymptomatic without signs of aerodigestive or vascular injury. When overt symptoms and/or signs are present, standard “ABC” resuscitation as described in the ATLS manual is performed. With moderate or modest symptoms or signs, a variety of diagnostic tests including cervical CT, conventional arteriography, duplex ultrasonography, color flow Doppler, CTA, esophagography, and fiber-optic esophagoscopy, tracheoscopy, and bronchoscopy are used to determine whether an injury to the carotid artery system, vertebral arteries, esophagus, or trachea is present.

When a BCVI is diagnosed, heparinization for Grade I–IV injuries and endovascular stenting, balloon occlusion, or operation for Grade V injuries are indicated. Prior to repeat imaging (CTA) in patients with Grade I–III injuries, aspirin and clopidogrel bisulfate are administered in anticipation of the need for an endovascular stent. Basic principles and techniques of arterial repair are used when penetrating carotid artery injuries are present. Temporary intraluminal shunts are only indicated if distal backflow is poor or if a prolonged complex repair is anticipated in Zone III. Penetrating unilateral vertebral artery injuries with hemorrhage are managed with packing, temporary balloon, or permanent occlusion or proximal and distal ligation.

Simple esophageal perforations are repaired with one or two layers of absorbable sutures. When there is a loss of esophageal tissue from one wall or a delay in diagnosis of an esophageal injury, a cervical loop esophagostomy is occasionally necessary.

Tracheal repairs for routine perforations are performed with one layer of absorbable sutures. A more significant anterior defect is managed with a tracheostomy at the first operation. When there is loss of the membranous trachea, a three-sided pericardial flap that is rotated superiorly will be necessary.

Diagnostic approaches and operative techniques have been refined significantly over the past 60 years, and this has resulted in a significant decrease in unnecessary operations and better outcomes after indicated operations.


1. Breasted JH. The Edwin Smith Surgical Papyrus. Chicago: University of Chicago Press; 1930.

2. Key G, ed. The Apologie and Treatise of Ambroise Pare containing the Ayages made into Divers Places with Many Writings upon Surgery. London: Falcon Education Books; 1957.

3. Fleming D. Case of rupture of the carotid artery; the wounds of several of its branches, successfully treated by tying the common trunk of the carotid itself. Med Chir J Rev. 1817;3:2.

4. Keevil JJ. David Fleming and the operation for ligation of the carotid artery. Br J Surg. 1949;37:92.

5. Eves A. Report of a case of suicidal wound of the throat with profuse haemorrhage successfully treated by ligature of the common carotid artery. Lancet. 1849;1:556.

6. Britt LD, Weireter LJ Jr, Cole FJ Jr. Management of acute neck injuries. In: Feliciano DV, Mattox KL, Moore EE, eds. Trauma. 6th ed. New York, NY: McGraw-Hill; 2008:467–476.

7. Monson DO, Saletta JD, Freeark RJ. Carotid vertebral trauma. J Trauma. 1969;9:987.

8. Roon AJ, Christensen N. Evaluation and treatment of penetrating cervical injuries. J Trauma. 1979;19:391.

9. Shearer VE, Giesecke AH. Airway management for patients with penetrating neck trauma: a retrospective study. Anesth Analg. 1993;77:1135.

10. Mandavia DP, Qualls S, Rokos I. Emergency airway management in penetrating neck trauma. Ann Emerg Med. 2000;35:221.

11. Feliciano DV. Management of penetrating injuries to carotid artery. World J Surg. 2001;25:1028.

12. Feliciano DV, Burch JM, Mattox KL, et al. Balloon catheter tamponade in cardiovascular wounds. Am J Surg. 1990;160:583.

13. Ball CG, Wyrzykowski AD, Nicholas JM, et al. A decade’s experience with balloon catheter tamponade for the control of hemorrhage. J Trauma. 2011;70:330.

14. Rostomily RC, Newell DW, Grady MS, et al. Gunshot wounds of the internal carotid artery at the skull base: management with vein bypass grafts and a review of the literature. J Trauma. 1997;42:123.

15. Cox MW, Whittaker DR, Martinez C, et al. Traumatic pseudoaneurysms of the head and neck: early endovascular intervention. J Vasc Surg. 2007;46:1227.

16. Herrera DA, Vargas SA, Dublin AB. Endovascular treatment of penetrating traumatic injuries of the extracranial carotid artery. J Vasc Interv Radiol. 2011;22:28.

17. Eddy VA. Is routine arteriography mandatory for penetrating injuries to Zone 1 of the neck? J Trauma. 2000;48:208.

18. Gasparri MG, Lorelli DR, Kralovich KA, et al. Physical examination plus chest radiology in penetrating periclavicular trauma: the appropriate trigger for angiography. J Trauma. 2000;49:1029.

19. Gracias VH, Reilly PM, Philpott J, et al. Computed tomography in the evaluation of penetrating neck trauma. A preliminary study. Arch Surg. 2001;136:1231.

20. Fogelman MJ, Stewart RD. Penetrating wounds of the neck. Am J Surg. 1956;91:581.

21. Bishara RA, Pasch AR, Douglas DD. The necessity of mandatory exploration of penetrating zone II neck injuries. Surgery. 1986;100:655.

22. Asensio JA, Valenziano CP, Falcone RE, et al. Management of penetrating neck injuries. The controversy surrounding zone II injuries. Surg Clin North Am. 1991;71:267.

23. Rao PM, Bhatti MF, Gaudino J, et al. Penetrating injuries of the neck: criteria for exploration. J Trauma. 1983;23:47.

24. Dunbar LL, Adkins RB, Waterhouse G. Penetrating injuries to the neck. Selective management. Am Surg. 1984;50:198.

25. Narrod JA, Moore EE. Selective management of penetrating neck injuries. A prospective study. Arch Surg. 1984;119:574.

26. Ayuyao AM, Kaledzi YL, Parsa MH, et al. Penetrating neck wounds. Mandatory versus selective exploration. Ann Surg. 1985;202:563.

27. Cohen ES, Breaux CW, Johnson PN, et al. Penetrating neck injuries: experience with selective exploration. South Med J. 1987;80:26.

28. Wood J, Fabian TC, Mangiante EC. Penetrating neck injuries: recommendations for selective management. J Trauma. 1989;29:602.

29. Gerst PH, Sharma SK, Sharma PK. Selective management of penetrating neck trauma. Am Surg. 1990;56:553.

30. Ngakane H, Muckart DJJ, Luvuno FM. Penetrating visceral injuries of the neck: results of a conservative management policy. Br J Surg. 1990; 77:908.

31. Mansour MA, Moore EE, Moore FA, et al. Validating the selective management of penetrating neck wounds. Am J Surg. 1991;162:517.

32. Demetriades D, Charalambides D, Lakhoo M. Physical examination and selective conservative management in patients with penetrating injuries of the neck. Surgery. 1993;80:1534.

33. Atteberry LR, Dennis JW, Menawat SS, et al. Physical examination alone is safe and accurate for evaluation of vascular injuries in penetrating zone II neck trauma. J Am Coll Surg. 1994;179:657.

34. Sekharan J, Dennis JW, Veldenz HC. Continued experience with physical examination alone for evaluation and management of penetrating zone 2 neck injuries: results of 145 cases. J Vasc Surg. 2000;32:483.

35. Azuaje RE, Jacobson LE, Glover J, et al. Reliability of physical examination as a predictor of vascular injury after penetrating neck trauma. Am Surg. 2003;69:804.

36. Mazolewski PJ, Curry JD, Browder T, et al. Computed tomography scan can be used for surgical decision making in zone II penetrating neck injuries. J Trauma. 2001;51:315.

37. Gonzalez RP, Falimirski M, Holevar MR, et al. Penetrating zone II neck injury: does dynamic computed tomographic scan contribute to the diagnostic sensitivity of a physical examination for surgically significant injury? A prospective blinded study. J Trauma. 2003;54:61.

38. Inaba K, Munera F, McKenney M, et al. Prospective evaluation of screening multislice helical computed tomographic angiography in the initial evaluation of penetrating neck injuries. J Trauma. 2006;61:144.

39. Sclafani SJ, Cavaliere G, Atweh N, et al. The role of angiography in penetrating neck trauma. J Trauma. 1991;31:557.

40. North CM, Ahmad J, Segall HD, et al. Penetrating vascular injuries of the face and neck: clinical and angiographic correlation. AJNR Am J Neuroradiol. 1986;7:855.

41. Menawat SS, Dennis JW, Laneve LM, et al. Are arteriograms necessary in penetrating zone II neck injuries? J Vasc Surg. 1992;16:397.

42. Blackshear WM, Phillips DJ, Thiele BL, et al. Detection of carotid occlusive disease by ultrasonic imaging and pulsed Doppler spectrum analysis. Surgery. 1979;86:698.

43. Strandress DE Jr. History of ultrasonic duplex scanning. Cardiovasc Surg. 1996;4:273.

44. Meissner M, Paun M, Johansen K. Duplex scanning for arterial trauma. Am J Surg. 1991;161:552.

45. Bynoe RP, Miles WS, Bell RM, et al. Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg. 1991;14:346.

46. Fry WR, Dort JA, Smith RS, et al. Duplex scanning replaces arteriography and operative exploration in the diagnosis of potential cervical vascular injury. Am J Surg. 1994;168:693.

47. Ginzburg E, Montalvo B, LeBlang S, et al. The use of duplex ultrasonography in penetrating neck trauma. Arch Surg. 1996;131:691.

48. Kuzniec A, Kaufman P, Molnar LJ, et al. Diagnosis of limbs and neck arterial trauma using duplex ultrasonography. Cardiovasc Surg. 1998;6:358.

49. Demetriades D, Theodorou D, Cornwell E III, et al. Penetrating injuries of the neck in patients in stable condition. Physical examination, angiography, or color flow Doppler imaging. Arch Surg. 1995;130:971.

50. Demetriades D, Theodorou D, Cornwell E, et al. Evaluation of penetrating injuries of the neck: prospective study of 223 patients. World J Surg. 1997;21:41.

51. Munera F, Soto JA, Palacio D, et al. Diagnosis of arterial injuries caused by penetrating trauma to the neck: comparison of helical CT angiography and conventional angiography. Radiology. 2000;216:356.

52. Munera F, Soto JA, Palacio DM, et al. Penetrating neck injuries: helical CT angiography for initial evaluation. Radiology. 2002;224:366.

53. Woo K, Magner DP, Wilson MT, et al. CT angiography in penetrating neck trauma reduces the need for operative neck exploration. Am Surg. 2005;71:754.

54. Emmett KP, Fabian TC, DiCocco JM, et al. Improving the screening criteria for blunt cerebrovascular injury: the appropriate role for computed tomography angiography. J Trauma. 2011;70:1058.

55. Bagheri SC, Khan HA, Bell RB. Penetrating neck injuries. Oral Maxillofac Surg Clin North Am. 2008;20:393.

56. Bryant AS, Cerfolio RJ. Esophageal trauma. Thorac Surg Clin. 2007;17:63.

57. Wu JT, Mattox KL, Wall MJ. Esophageal perforations: new perspectives and treatment paradigms. J Trauma. 2007;63:1173.

58. Defore WW Jr, Mattox KL, Hansen HA, et al. Surgical management of penetrating injuries of the esophagus. Am J Surg. 1977;134:734.

59. Symbas PN, Hatcher CR Jr, Vlasis SE. Esophageal gunshot wounds. Ann Surg. 1980;191:703.

60. Armstrong WB, Detar TR, Stanley RB. Diagnosis and management of external penetrating esophageal injuries. Ann Otol Rhinol Laryngol. 1994;103:868.

61. Weigelt JA, Thal ER, Snyder WH, et al. Diagnosis of penetrating cervical esophageal injuries. Am J Surg. 1987;154:619.

62. Flowers JL, Graham SM, Ugarte MA, et al. Flexible endoscopy for the diagnosis of esophageal trauma. J Trauma. 1996;40:261.

63. Arantes V, Campolina C, Valerio SH, et al. Flexible esophagoscopy as a diagnostic tool for traumatic esophageal injuries. J Trauma. 2009;z66:1677.

64. Hermon A, Segal K, Har-el G, et al. Complete cricotracheal separation following blunt trauma to the neck. J Trauma. 1987;27:1365.

65. Grover FL, Ellestad C, Arom KV, et al. Diagnosis and management of major tracheobronchial injuries. Ann Thorac Surg. 1979;28:384.

66. Lyons JD, Feliciano DV, Wyrzykowski AD, et al. Modern management of penetrating tracheal injuries. Am Surg. In press.

67. Scalfani SJ, Panetta T, Goldstein AS, et al. The management of arterial injuries caused by penetration of zone III of the neck. J Trauma. 1985;25:871.

68. Ferguson E, Dennis JW, Vu JH, et al. Redefining the role of arterial imaging in the management of penetrating zone 3 neck injuries. Vascular. 2005;13:158.

69. Biffl WL, Moore EE, Rehse DH, et al. Selective management of penetrating neck trauma based on cervical level of injury. Am J Surg. 1997;174:678.

70. Rivers SP, Patel Y, Delany HM, et al. Limited role of arteriography in penetrating neck trauma. J Vasc Surg. 1988;8:112.

71. Mulloy JP, Flick PA, Gold RE. Blunt carotid injury: a review. Radiology. 1998;207:571.

72. Verneuil M. Contusions multiples: delire violent; hemiplegie a droite, signes decompression cerebrale. Bull Acad Natl Med (Paris). 1872;36:46 [cited in Ref.71].

73. Welling RE, Saul TG, Tew JM Jr, et al. Management of blunt injury to the internal carotid artery. J Trauma. 1987;27:1221.

74. Davis JW, Holbrook TL, Hoyt DB, et al. Blunt carotid artery dissection: incidence, associated injuries, screening, and treatment. J Trauma. 1990;30:1514.

75. Biffl WL, Moore EE, Elliott JP, et al. Blunt cerebrovascular injuries. Curr Probl Surg. 1999;36:505.

76. Feliciano DV. Patterns of injury. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. 3rd ed. Stamford, CT: Appleton & Lange; 1996: 85–103.

77. Kerwin AJ, Bynoe RP, Murray J, et al. Liberalized screening for blunt carotid and vertebral artery injuries is justified. J Trauma. 2001;51:308.

78. Berne JD, Norwood SH, McAuley CE, et al. The high morbidity of blunt cerebrovascular injury in an unscreened population: more evidence of the need for mandatory screening protocols. J Am Coll Surg. 2001; 192:314.

79. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries. Analysis of diagnostic modalities and outcomes. Ann Surg. 2002;236:386.

80. Cothren CC, Moore EE, Ray CE, et al. Screening for blunt cerebrovascular injuries is cost-effective. Am J Surg. 2005;190:845.

81. Ringer AJ, Matern E, Parikh S, et al. Screening for blunt cerebrovascular injury: selection criteria for use of angiography. J Neurosurg. 2010; 112:1146.

82. Berne JD, Cook A, Rowe SA, et al. A multivariate logistic regression and analysis of risk factors for blunt cerebrovascular injury. J Vasc Surg. 2010; 51:57.

83. Cook A, Osler T, Gaudet M, et al. Blunt cerebrovascular injury is poorly predicted by modeling with other injuries: analysis of NTDB data. J Trauma. 2011;71:114.

84. Fabian, TC, Patton JH Jr, Croce MA, et al. Blunt carotid injury. Importance of early diagnosis and anticoagulant therapy. Ann Surg. 1996;223:513.

85. Berne JD, Reuland KS, Villarreal DH, et al. Sixteen-slice multi-detector computed tomographic angiography improves the accuracy of screening for blunt cerebrovascular injury. J Trauma. 2006;60:1204.

86. Eastman AL, Chason DP, Perez CL, et al. Computed tomographic angiography for the diagnosis of blunt cervical vascular injury: is it ready for primetime? J Trauma. 2006;60:925.

87. Biffl WL, Egglin T, Benedetto B, et al. Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma. 2006; 60:745.

88. Goodwin RB, Beery PR II, Dorbish RJ, et al. Computed tomographic angiography versus conventional angiography for the diagnosis of blunt cerebrovascular injury in trauma patients. J Trauma. 2009;67:1046.

89. Sliker CW, Shanmuganathan K, Mirvis SE. Diagnosis of blunt cerebrovascular injuries with 16-MDCT: accuracy of whole-body MDCT compared with neck MDCT angiography. AJR Am J Roentgenol. 2008;190:790.

90. DiCocco JM, Emmett KP, Fabian TC, et al. Blunt cerebrovascular injury screening with 32-channel multidetector computed tomography: more slices still don’t cut it. Ann Surg. 2011;253:444.

91. Ren X, Wang W, Zhang X, et al. Clinical study and comparison of magnetic resonance angiography (MRA) and angiography diagnosis of blunt vertebral artery injury. J Trauma. 2007;63:1249.

92. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid arterial injuries: implications of a new grading scale. J Trauma. 1999;47:845.

93. Norwood SH, Berne JD, Rowe SA, et al. Early venous thromboembolism prophylaxis with enoxaparin in patients with blunt traumatic brain injury. J Trauma. 2008;65:1021.

94. Cothren CC, Moore EE, Biffl WL, et al. Anticoagulation is the gold standard therapy for blunt carotid injuries to reduce stroke rate. Arch Surg. 2004;139:540.

95. Wahl WL, Brandt MM, Thompson BG, et al. Antiplatelet therapy: an alternative to heparin for blunt cardiac injury. J Trauma. 2002; 52:896.

96. Kerby, JD, May AK, Gomez CR, et al. Treatment of bilateral blunt carotid injury using percutaneous angioplasty and stenting: case report and review of the literature. J Trauma. 2000;49:784.

97. Brandt MM, Kazanjian S, Wahl WL. The utility of endovascular stents in the treatment of blunt arterial injuries. J Trauma. 2001;51:901.

98. Duane TM, Parker F, Stokes GK, et al. Endovascular carotid stenting after trauma. J Trauma. 2002;52:149.

99. Diaz-Daza O, Arraiza FJ, Barkley JM, et al. Endovascular therapy of traumatic vascular lesions of the head and neck. Cardiovasc Intervent Radiol. 2003;26:213.

100. Cothren CC, Moore EE, Ray CE, et al. Carotid artery stents for blunt cerebrovascular injury. Risks exceed benefits. Arch Surg. 2005;140:480.

101. Joo JY, Ahn JY, Chung YS, et al. Therapeutic endovascular treatments for traumatic carotid artery injuries. J Trauma. 2005;58:1159.

102. Cohen JE, Ben-Hur T, Rajz G, et al. Endovascular stent-assisted angioplasty in the management of traumatic internal carotid artery dissections. Stroke. 2005;36:45.

103. Edwards NM, Fabian TC, Claridge JA, et al. Antithrombotic therapy and endovascular stents are effective treatment for blunt carotid injuries: results from longterm followup. J Am Coll Surg. 2007;204:1007.

104. DuBose J, Recinos G, Teixeira PGR, et al. Endovascular stenting for the treatment of traumatic internal carotid injuries: expanding experience. J Trauma. 2008;65:1561.

105. Li W, D’Ayala M, Hirshberg A, et al. Comparison of conservative and operative treatment for blunt carotid injuries: analysis of the national trauma data bank. J Vasc Surg. 2010;51:593.

106. Liekweg WG Jr, Greenfield LJ. Management of penetrating carotid arterial injury. Ann Surg. 1978;188:587.

107. Ledgerwood AM, Mullins RJ, Lucas CE. Primary repair vs. ligation for carotid artery injuries. Arch Surg. 1980;115:488.

108. Brown MF, Graham JM, Feliciano DV, et al. Carotid artery injuries. Am J Surg. 1982;144:748.

109. Weaver FA, Yellin AE, Wagner WH, et al. The role of arterial reconstruction in penetrating carotid injuries. Arch Surg. 1988; 123:1106.

110. Feliciano DV. A new look at penetrating carotid artery injuries. In: Maull KI, Cleveland HC, Feliciano DV, et al., eds. Advances in Trauma and Critical Care. Vol. 9. St. Louis, MO: Mosby-Year Book; 1994:319–345.

111. Ramadan F, Rutledge R, Oller D, et al. Carotid artery trauma: a review of contemporary trauma center experiences. J Vasc Surg. 1995;21:46.

112. Teehan EP, Padberg FT Jr, Thompson PN, et al. Carotid arterial trauma: assessment with the Glasgow Coma Scale (GCS) as a guide to surgical management. Cardiovasc Surg. 1997;5:196.

113. Dichtel WJ, Miller RH, Woodson GE, et al. Lateral mandibulotomy: a technique of exposure of penetrating injuries of the internal carotid artery at the base of the skull. Laryngoscope. 1984;94:1140.

114. Fisher DF Jr, Clagett GP, Parker JI, et al. Mandibular subluxation for high carotid exposure. J Vasc Surg. 1984;1:727.

115. Dossa C, Shepard AD, Wolford DG, et al. Distal internal carotid exposure: a simplified technique for temporary mandibular subluxation. J Vasc Surg. 1990;12:319.

116. Simonian GT, Pappas RJ, Padberg FT Jr, et al. Mandibular subluxation for distal internal carotid exposure: technical considerations. J Vasc Surg. 1999;30:1116.

117. Jaspers GW, Witjes MJ, van den Dungen JJ, et al. Mandibular subluxation for distal internal carotid artery exposure in edentulous patients. J Vasc Surg. 2009;50:1519.

118. Kumins NH, Tober JC, Larsen PE, et al. Vertical ramus osteotomy allows exposure of the distal internal carotid artery to the base of the skull. Ann Vasc Surg. 2001;15:25.

119. Bradley EL III. Management of penetrating carotid injuries: an alternative approach. J Trauma. 1973;13:248.

120. Waldman DL, Barquist E, Poynton FG, et al. Stent graft of a traumatic vertebral artery injury: case report. J Trauma. 1998;44:1094.

121. Albuquerque FC, Javedan SP, McDougall CG. Endovascular management of penetrating vertebral artery injuries. J Trauma. 2002;53:574.

122. Meier DE, Brink BE, Fry WJ. Vertebral artery trauma: acute recognition and treatment. Arch Surg. 1981;116:236.

123. Golueke P, Sclafani S, Phillips T, et al. Vertebral artery injury—diagnosis and management. J Trauma. 1987;27:856.

124. Reid JDS, Weigelt JA. Forty-three cases of vertebral artery trauma. J Trauma. 1988;28:1007.

125. Blickenstaff KL, Weaver FA, Yellin AE, et al. Trends in the management of traumatic vertebral artery injuries. Am J Surg. 1989;158:101.

126. Popovsky J, Lee YC, Berk JL. Gunshot wounds of the esophagus. J Thorac Cardiovasc Surg. 1976;72:609.

127. Cheadle W, Richardson JD. Options in management of trauma to the esophagus. Surg Gynecol Obstet. 1982;155:380.

128. Winter RP, Weigelt JA. Cervical esophageal trauma. Arch Surg. 1990; 125:849.

129. Asensio JA, Chahwan S, Forno W, et al. Penetrating esophageal injuries: multicenter study of the American Association for the Surgery of Trauma. J Trauma. 2001;50:289.

130. Rigberg DA, Centeno JM, Blinman TA, et al. Two decades of cervical esophagostomy: indications and outcomes. Am Surg. 1998;64:939.

131. Koniaris LG, Spector SA, Staveley-O’Carroll KF. Complete esophageal diversion: a simplified, easily reversible technique. J Am Coll Surg. 2004;199:991.

132. Symbas PN, Hatcher CR, Boehm GAW. Acute penetrating tracheal trauma. Ann Thorac Surg. 1976;22:473.

133. Montgomery WW. Suprahyoid release for tracheal anastomosis. Arch Otolaryngol. 1974;99:255.

134. Feliciano DV, Bitondo CG, Mattox KL, et al. Combined tracheoesophageal injuries. Am J Surg. 1985;150:710.

135. Losken A, Rozycki GS, Feliciano DV. The use of the sternocleidomastoid muscle flap in combined injuries to the esophagus and carotid artery or trachea. J Trauma. 2000;49:815.