Two fascial layers invest the neck: the superficial fascia enveloping the platysma muscle and the deep cervical fascia. Musculoskeletal structures at risk include the cervical spine; cervical muscles, tendons, and ligaments; clavicles; first and second ribs; and hyoid bone. Neural structures at risk include the spinal cord, phrenic nerve, brachial plexus, recurrent laryngeal nerve, cranial nerves (specifically IX-XII), and stellate ganglion. Vascular structures at risk include the carotid (common, internal, external) and vertebral arteries and the vertebral, brachiocephalic, and jugular (internal and external) veins. Visceral structures at risk include the thoracic duct, esophagus and pharynx, and larynx and trachea. Glandular structures at risk include the thyroid, parathyroid, submandibular, and parotid glands.

Generally, people with GSWs sustain greater injury than those with stab wounds because of a bullet's proclivity to penetrate deeper and cause cavitation, damaging structures lying outside the tract of the missile. Bullets tend to course randomly and follow a more direct pathway. GSWs, particularly those involving high-velocity bullets (>2000-2500 ft/s) produced by military-style weapons or hunting rifles, generate shock waves that devitalize surrounding tissues. High-velocity missiles and their ensuing blast effects may suck debris into the wound tract or cause secondary injuries from bullet or bone fragmentation. Low-velocity injuries may be produced by .22- and . 38-caliber handguns that have a muzzle speed of 800 ft/s.

A transcervical GSW is more likely to cause a grave injury than a GSW involving injury to only 1 side of the neck. Close-range GSWs of the neck that produce massive destruction are usually fatal. After a GSW to the neck, surgery is indicated in 75% of cases, while only 50% of neck stab wounds require surgical exploration.

Vascular injuries arising from penetrating trauma may occur directly, causing a partial or complete transection of the vessel or inducing formation of an intimal flap, arteriovenous fistula, or pseudoaneurysm. Blood vessel injury results from external compression, mural contusion, or thrombosis and is the most prevalent disorder arising from penetrating trauma, occurring in 25-40% of patients. The internal jugular vein (9%) and carotid artery (7%) are the most common sites of vascular injuries. Injury to the pharynx or the esophagus occurs in 5-15% of cases. The larynx or the trachea is injured in 4-12% of cases. Major nerve injury occurs in 3-8% of patients sustaining penetrating neck trauma. Spinal cord injury occurs infrequently and almost always results from direct injury rather than secondary osseous instability.

Blunt trauma to the neck typically results from motor vehicle accidents, but it also occurs with sports-related injuries (e.g.: clothesline tackle), strangulation, blows from the fists or feet, and excessive manipulation (i.e.: any manual operation, such as chiropractic treatment or physical realignment or repositioning of the spine).

In motor vehicle accidents in which the driver is not belted, the driver is in danger of thrusting forward with the head extended, forcing the anterior neck against the steering column. Shoulder harnesses appear to offer some, though incomplete, protection against blunt neck trauma; cerebral vessel and laryngeal injuries secondary to shoulder strap compression have occurred.

Nonpenetrating trauma can injure a blood vessel through a multitude of mechanisms. Direct forces can shear the vasculature. Excessive rotation and/or hyperextension of the cervical spine causes distention and stretching of the arteries and veins to the point of rupture. Intraoral trauma may extend to the blood supply. Basilar skull fractures may disrupt the intrapetrous portion of the carotid artery.

Impact to the exposed anterior aspect of the neck may crush the larynx or the trachea, particularly at the cricoid ring, and compress the esophagus against the posterior spinal column. A sudden increase in intratracheal pressure against a closed glottis (e.g.: improper wearing of a seat belt), a crush bruise (e.g.: clothesline tackle), or a rapid acceleration- deceleration action may cause a tracheal injury.

Strangulation may result from hanging (partial or complete suspension of the body from the neck), ligature suffocation, manual choking, and postural asphyxiation (e.g.: seen in children when the neck is placed over an object and the body weight produces compression). Significant cervical spine and spinal cord damage happens in only those hangings that involve a fall from a distance greater than the body height. Simple asphyxiation is not the major cause of death in hanging injuries. Cervical spinal disruption subsequent to strangulation is almost uniformly fatal.

• Use all available sources when trying to establish the mechanism of injury. Question the patient, involved bystanders, and prehospital personnel. Clarify events surrounding the traumatic event, establish the amount of time that elapsed since the injury, and confirm the patient's baseline condition. Determine the amount of blood that was lost at the scene and whether the patient lost consciousness. Determine if any evidence of recent drug or alcohol ingestion is present.




• When neck trauma results from a motor vehicle accident, inquire about seat belt use, location of the patient in the car (driver or front or back seat passenger), deployment of an air bag, and magnitude of car damage (e.g.: intrusion, steering column and windshield intact or broken).




• In the event of a penetrating trauma, try to verify details about the weapon used, such as type and size of knife or type and caliber of gun.




• For patients with injuries due to hanging, try to determine the suspension time (when the patient was last seen), drop height, ligature used, history of alcohol or drug abuse, and history of suicide attempts.




• Characterize pain (e.g.: location, nature, intensity, onset, radiation), and document the nature and location of all stated injuries.




• Cardiovascular manifestations range from bleeding to symptoms normally associated with a cerebrovascular accident.




• Symptoms relating to the aerodigestive tract include dyspnea, hoarseness, dysphonia, and dysphagia.




• CNS problems include paresthesias, weakness, plegia, and paresis.

Search the neck for a breach of the platysma. Invested by the most superficial fascia, the platysma serves as the harbinger for serious penetrating neck wounds. Any violation of the platysmal muscle should alert the physician to the potential for grave damage to the contents of the neck. If the platysma is violated, judge whether the wound lies anterior (anterior triangle) or posterior (posterior triangle) to the sternocleidomastoid muscle, and determine in what zone the injury is found. Try to specify the direction of the wound tract (e.g.: toward or away from the midline or clavicle). Half of the cases of penetrating neck trauma in which the platysma is violated have no further injury. If the platysma clearly is not violated by a penetrating injury, the patient can be safely cleared of a significant underlying injury.

Consider an arterial injury of the neck in patients manifesting gross bleeding; a hematoma; asymmetry of arterial pulses; a new bruit on auscultation; neurological deficits, especially lateralizing cerebral findings; or hypotension. Do not unnecessarily probe or manipulate the wound or perform any action that may cause the patient to gag, choke, or cough. Any of these reactions may dislodge a clot and provoke a life-threatening hemorrhage. Hard signs of an arterial injury include a large expanding hematoma, severe active or pulsatile bleeding, shock unresponsive to fluids, signs of cerebral infarction, presence of a bruit or thrill, and diminished distal pulses. Virtually all patients with hard signs of an arterial injury require operative repair. Soft signs, such as a nonexpanding hematoma and paresthesias, do not improve the predictive value of an arterial injury more than indicating the proximity of the wound to a major vessel. The presence of a pulse does not exclude a vascular injury, nor is absence of a pulse diagnostic of vascular damage. Clinical findings are lacking initially in almost one third of patients with an arterial injury of the neck. Nearly one third of carotid artery injuries are associated with a central neurological deficit.

Perforation of the pharynx or the esophagus following blunt neck trauma rarely occurs. Initially, the patient may have no complaints, and the physical examination fails to reveal injury. Since the wall of the esophagus is fragile, iatrogenic injury can follow endoscopy, passage of a nasogastric tube, or inadvertent esophageal intubation. Esophageal perforation is the most serious and rapidly fatal trauma-induced perforation of the gastrointestinal tract.

Brachial plexus injuries sustained from blunt trauma tend to involve the upper nerve roots (C5 to C7), diminishing the capacity of the upper arm while sparing strength and sensation of the lower arm. A radical avulsion of the brachial plexus results in a flaccid, numb extremity. Quadriplegia occurring with complete transection of the spinal cord manifests as an absence of all motor, sensory, and reflex function below the level of injury. Bilateral neurological findings imply a spinal cord injury until proven differently. Brown-Séquard syndrome results from hemisection of the spinal cord, causing ipsilateral motor paralysis with contralateral sensory deficits.

• Laryngoscopy, bronchoscopy, pharyngoscopy, and esophagoscopy may be useful in the assessment of the aerodigestive tract. Rigid endoscopes are superior to flexible scopes.




• Before inserting any scope, confirm that the airway is patent, intact, and protected (usually ensured by placement of an endotracheal tube). Ecchymosis of the posterior or lateral pharyngeal wall implies concealed neck damage.




• Endoscopy, especially indirect laryngoscopy, often becomes problematical in the apprehensive trauma patient, and it may be best to defer examination until the airway is protected and the patient is anesthetized.

• Angiography routinely is employed to evaluate stable patients sustaining penetrating wounds to zones I and III that pierce the platysma. Angiography remains preferred to alternative contrast studies because it is less likely to obscure vascular damage.




• A 4-vessel study is a prerequisite.




• Preoperative arteriograms facilitate operative decision making, particularly when a question of intrathoracic involvement exists (such as with zone I injuries necessitating a thoracotomy). Otherwise, consider confirming adequacy of the collateral circulation if carotid artery ligation is contemplated (as may be necessary in zone III arterial wounds). Never send an unstable patient to a radiographic suite.

Consult an experienced trauma surgeon emergently once platysmal violation is confirmed. Additional consultants should be prioritized with guidance from the trauma surgeon who will oversee the patient's care. Ordinarily, urgent surgical exploration of a penetrating wound to the neck is indicated for the following:

• Continued blood loss, expanding hematoma, hypovolemic shock, and/or pulse deficit




• Airway obstruction, impending airway obstruction, open trachea, and/or air bubbling from the wound site




• Neurologic deficit




• Blood in the aerodigestive tract, hemoptysis, and/or hematemesis




• New-onset bruit

Infection subsequent to penetrating wounds of the neck is a major cause of death and disability. Administering prophylactic antibiotics, while not decisively validated by scientific studies, should be a consideration. Recommended medications vary from penicillin to those with broad-spectrum coverage. Factors to consider include the physical nature of the injury (e.g.: simple laceration vs blunt trauma with tearing-type injuries). If prophylactic antibiotics are to be effective, attempt to obtain adequate tissue levels immediately, preferably within 4 h of injury.

Other therapeutic agents to consider are the corticosteroids. Massive doses of steroids are believed to have possible benefit in improving neurological function in selected subsets of patients. In the second phase of a benchmark study (Bracken et al), patients who had sustained blunt spinal injury within a 12-h time frame were given a 30 mg/kg IV bolus of corticosteroids followed by 5.4 mg/kg/h for 23 h. Overall, patients who appropriately received steroids within 8 h revealed slight improvement in function in motor and sensory function at 6 mo. Other experimental agents include naloxone, dimethylsulfoxide, and growth factors. Spinal cooling also has been proposed.