A previously healthy 30-year-old male was shot at close range with a low caliber hand gun. A 911 call was placed immediately and paramedics were on the scene within 10 minutes. The victim was fully awake and cooperative. There was a single gunshot entrance wound in the midline at the level of the thyroid cartilage (Figure 37–1). The entry wound was about 5 mm in diameter and air was noted to be escaping from it. There was minimal bleeding. The patient complained of pain in the area of the anterior neck and the left scapula. He also complained of dyspnea and coughed up scant bloody sputum. He had no allergies, was on no medications, and was previously healthy.

Vital signs at the scene were: BP 140/60 mm Hg, HR 90 beats per minute, RR 22 breaths per minute. Oxygen saturation (SaO₂) was 97% and the Glasgow coma scale was 15. One intravenous cannula was placed in each upper extremity and oxygen was administered by non-rebreathing face mask (NRFM). The patient was immobilized on a spine board and transported to the emergency department (ED). Transport time was 20 minutes.

On arrival in the ED the patient was awake and responded appropriately. Vital signs were: BP 140/90 mm Hg, HR 98 beats per minute, RR 26 breaths per minute. SaO₂ was 98% on NRFM. He was hoarse, had scant hemoptysis, and complained of pain in the anterior neck and left scapular area. Air could again be appreciated escaping from the neck wound. There was minimal bleeding. Subcutaneous (SC) emphysema was palpable in the anterior neck but no hematoma was detected. No exit wound was identified. Air entry was decreased on auscultation of the left chest. The Glasgow Coma scale was 15 and there were no neurologic deficits. The remainder of the examination was unremarkable.

How Common Is Penetrating Neck Injury (PNI)?

PNI has been reported to occur in 0.98% to 10% of all trauma patients^1–6 and in 0.4% to 5% of major penetrating trauma.⁷ Up to one-third of PNIs are accompanied by other moderate to severe injury.¹ Not all PNIs involve vital structures. In a review of 26 reported series with a total of 4193 patients with PNI, there were 1285 vascular injuries (31%), 331 laryngotracheal injuries (8%), and 354 digestive (pharyngeal and esophageal) injuries (8.4%).⁸ Others have reported vascular injury in 13.3% to 37% of PNIs,^3,9–13 aerodigestive tract injury in 5% to 18.5%,^{5,9,11,13–15} and esophageal injury in 0.9% to 9.6%.^9,12,14,16 Pharyngoesophageal injury has been reported in 8% and 8.9% of PNIs,^11,13 and spinal cord injury in 3.2%⁴ and 6.7%.¹⁰ The incidence of unstable cervical spine injury after penetrating neck trauma has been reported to be 0.4%.⁴ Approximately 16% of gunshot wounds (GSWs) to the neck and 14% of stab wounds (SWs) are associated with a hemo/pneumothorax.^10,17

What Is the Mortality Associated with PNI?

The mortality associated with PNI has been reported in multiple series and reviews to be between 0% and 17%^{1,4–6,8–12,18–29} with most of the fatalities resulting from vascular injury.^1,5,11

Two series of patients with PNI have reported the mortality associated with vascular injury to be 0%¹³ and 2.2%.¹⁰ However, a mortality of 10% to 30% and approaching 50% has also been quoted.^3,19,30 In a review of 11 series with a total of 1584 cases, Asensio et al.⁸ reported an average calculated mortality from penetrating carotid injury of 17%.

The mortality associated with penetrating laryngotracheal trauma has been reported to be 13.5%,³¹ 3.5%,³² 0%,¹³ and 11.5%.³³ However, a mortality of 20%^6,34 to 40%³¹ has also been quoted.

The average calculated mortality for cervical esophageal wounds, most of which were penetrating, has been reported to be 10%.⁸ An increase in mortality has been observed with delayed diagnosis.³ A mortality of 22% has also been quoted for penetrating pharyngoesophageal injuries.⁶ A mortality associated with aerodigestive tract injury of 13% has also been reported.³⁵

The mortality associated with PNI also varies with the mechanism of injury.²⁸ The mortality associated with high-velocity bullet wounds is greater than that associated with low-velocity bullet wounds which is greater than that associated with SWs.²⁸ A mortality of 87% has been quoted for close range shotgun wounds (SGWs).³⁶

Why Is Knowledge of the Anatomy of the Neck Important in PNI?

The anatomy of the neck is complex with multiple vital structures in close proximity enveloped in tight fascial compartments.^5,17 No other region of the body contains so many vital structures in such a confined space. Penetrating injury to the aerodigestive tract, major vascular structures, and the spinal cord can be life threatening.⁹ Optimal evaluation and management requires a thorough knowledge of the local anatomy.^17,37

The neck can be defined as that area located between the lower margin of the mandible and the superior nuchal line of the occipital bone superiorly, and the suprasternal notch and the upper border of the clavicles inferiorly.³⁷ For the purpose of classification of PNI, the neck has been divided into three anatomic zones (Figure 37–2)^9,37 based on surgical accessibility to the underlying vasculature and aerodigestive tract structures.² Although Monson and others^38–41 have described the sternal notch as the boundary line between zones I and II, multiple other authors consider zone I to extend from the level of the clavicles and sternal notch to the cricoid cartilage,^{1,3,7,9,10,13,17,34,37,42–44} and zone II to extend from the level of the cricoid cartilage to the angle of the mandible. Zone III extends from the angle of the mandible to the base of the skull. Although the three zones of the neck have been said to refer to the area anterior to the sternocleidomastoid muscles,⁹ posterior neck structures have also been included in this classification.^9,37

The structures in zone I include the aortic arch, proximal carotid arteries, vertebral arteries, subclavian vessels, innominate vessels, apices of the lung, esophagus, trachea, brachial plexus, thoracic duct, and spinal cord (Figure 37–3). Important structures in zone II include the common, internal, and external carotids, the jugular veins, the larynx, the hypopharynx, and the spinal cord^3,9,37 (Figure 37–4). Important structures in zone III include the distal cervical, petrous, and cavernous portions of the internal carotid arteries, the vertebral arteries, the external carotid arteries and their major branches, the jugular veins, the prevertebral venous plexus, the pharynx, the spinal cord, and the facial nerves^3,9,37 (Figure 37–5).

The location of the external wound does not necessarily correlate with the location of the underlying injury² and the site of the wound itself is no longer felt to be a reliable indicator of the presence of an injury, or the structures injured.¹¹ The relevance of the zone classification in the modern management of PNI has been questioned and a “no zone” approach has been advocated.⁴⁴

The platysma, a thin superficial muscular sheet enclosed by the superficial fascia of the neck has often been cited as an important anatomical landmark in the determination of whether a penetrating neck wound is superficial or deep.^3,37 Penetration of the platysma raises the potential of injury to a vital structure, and has been used as an indication for neck exploration. Deep to platysma is the deep cervical fascia which is subdivided into the investing, pretracheal, and prevertebral layers.³ These fascial layers play an important role in the clinical presentation and complications following penetrating trauma.¹⁷ The fascial compartments of the neck can limit external hemorrhage, but when bleeding occurs within these closed compartments, airway compression and distortion can be precipitated (Figure 37–6).

What Do “Selective” and “Mandatory” Neck Exploration Mean?

Penetrating injuries in zones I and III present complex diagnostic and therapeutic challenges.⁵ Management of penetrating injury to zone I is complicated by difficult surgical exposure and difficult proximal control of bleeding vessels.³ Penetrating injury to zone III is similarly complicated by difficult surgical exposure and distal control of bleeding vessels.³ Operative intervention for injury in zones I and III has traditionally been selective, based on physical examination and radiologic findings.³⁷

The surgical management of penetrating injury to zone II has been controversial. Some authors have advocated mandatory exploration for wounds that penetrate the platysma, whereas others recommend a more selective approach to surgical exploration due to high negative exploration rates using the mandatory approach.^{10,13,16,18,20–23,25–28,45–51} Mandatory exploration was considered the standard of care for several decades after World War II.⁵ This practice has now been abandoned by most trauma centers and replaced by selective nonoperative management based on the clinical examination and appropriate investigations.¹⁷ There is now strong evidence that the clinical exam, preferably according to a written protocol, is very reliable in identifying highly suspecting significant injuries¹⁷ and can be used to triage patients directly to the OR, to observation, or to appropriate investigation.² Selective exploration is currently the standard of care.⁵²

Penetrating neck trauma most commonly occurs in zone II^17,29,36 and requires emergency airway intervention in about one-third of cases.²⁹ In a series of 223 patients with PNI, Demetriades et al.¹⁰ reported zone II injury in 47%, zone I injury in 18%, and zone III injury in 19%. More than one zone was involved in 16%. Inaba et al.² reported zone II injury in 38.2%, zone I injury in 16.9%, and zone III injury in 16% in a series of 453 PNIs. Multiple zones were involved in 28%. Two smaller series reported zone II injury in 43% to 64%, zone I injury in 16% to 17%, and zone III injury in 20% to 27%.^5,9 Soliman et al.⁵ reported injuries in multiple zones in 13%. In two series with predominantly SWs, most injuries occurred in zone I (41%–44%), followed by zone II (28%–29%), and zone III (7%–27%).^11,53 In the series reported by Madsen et al.,¹¹ 76% of the patients sustained wounds to the anterior triangle of the neck. Wounds in the anterior and lateral aspects of the neck produce airway compromise more often than those in the posterior region.⁵⁴ Most SWs are to the left side of the neck, presumably due to the predominance of right-handed assailants.¹⁷

What Are the Mechanisms of Injury in Penetrating Neck Trauma?

Eleven to 64% of PNIs that penetrate the platysma have been reported to be caused by GSWs, 29% to 89% by SWs, and 0.9% to 6% by SGWs.^{1,2,5,9–11,13} SWs produce a more predictable pattern of injury than do GSWs.³⁶

GSWs produce tissue destruction that is dependent on the kinetic energy of the projectile, which is a function of its velocity.³⁷ However, the transfer of kinetic energy is not the only determinant of tissue wounding.⁵⁵ Tissue disruption depends as much on the shape, size, construction, and mass of the projectile as on its velocity.^55,56 The pathophysiology of GSWs is complex and high-velocity projectiles do not necessarily cause more tissue damage than lower-velocity projectiles.^56,57 The definition of high velocity is also imprecise.^55,56 Caliber refers to the diameter of the projectile.⁵⁵ The projectile produces a crush effect on tissue that it contacts (the permanent cavity) and a stretch effect on tissue surrounding the missile path (the temporary cavity) produced by radial pressure waves which follow the penetrating projectile and impel the walls of the permanent cavity radially outwards.^55,56,58,59 The volume of the permanent cavity is influenced by the yaw or tumbling, deformation, and fragmentation of the projectile.⁵⁵ The volume of the temporary cavity, in general, increases with the velocity of the projectile, and increases if the projectile tumbles or fragments.⁶⁰ The effect of temporary cavitation is clinically variable and will depend on the elasticity of the tissue affected as tissue planes are separated and tissues are displaced and stretched beyond elastic limits.^55,57,59 Inelastic tissues such as liver are more susceptible to disruption by the temporary cavity than flexible tissue such as muscle.^57,59 When bullets strike bone they can also ricochet, fragment, and deviate to make the resultant wound unpredictable and more extensive.⁵⁷ The site of the entry wound should be identified as well as the exit wound (if present), and consideration should be given to the path of the projectile.³ GSWs are more likely to cause vascular, aerodigestive, and neurologic injuries than are SWs (73% vs. 31%).^3,10 In a prospective series of PNIs, GSWs were three times more likely than SWs to cause a large hematoma (20.6% vs. 6.7%); twice as likely to be associated with hypotension on admission (13.4% vs. 7.9%); twice as likely to cause a vascular injury (26.8% vs. 14.6%); twice as likely to injure aerodigestive structures (7.2% vs. 3.4%); and 13 times more likely to cause spinal cord injury (13.4% vs. 3.4%).^10,17 Overall approximately 35% to 45% of GSWs and 20% to 23% of SWs to the neck produce significant injuries to vital structures.^17,36,61 Transcervical GSWs (those that cross the midline) are more likely to injure vital structures than GSWs that do not cross the midline.^3,24 Seventy-three percent of transcervical GSWs are associated with significant injuries to vital structures.^17,62 For this reason, mandatory exploration of transcervical wounds has been recommended,⁶³ while others continue to recommended a selective approach.^17,24,62

PNI can produce airway compromise as a result of blood and debris in the airway lumen, laryngotracheal injury with obstruction and air leak, and external compression by hematoma, edema, or SC emphysema.^17,54 Spinal cord injury can also cause respiratory distress. Airway management is guided by clinical presentation.⁶

What Are the Essential Elements of the Clinical Evaluation of PNI?

Historically, physical examination of a PNI was considered to be unreliable unless hard signs of injury were present.¹ However, more recently it has been shown that a structured clinical examination can be used to triage patients regardless of the zone of injury.² Patients can be categorized into those with hard signs, soft signs, and no signs of vascular or aerodigestive injury.² The initial evaluation should follow the standard ABCs of resuscitation, followed by a systematic, rapid, and thorough secondary survey.³ The primary survey should identify or rule out airway obstruction, tension pneumothorax, major active bleeding, spinal cord injury, and ischemic brain injury.¹⁷ The secondary survey is directed to the identification of signs and symptoms of occult vascular injury, occult laryngotracheal injury, pharyngoesophageal injury, cranial and peripheral nerve injuries, and small pneumothoraces.¹⁷ Presence of “hard” signs of vascular or laryngotracheal injury including an expanding or pulsatile hematoma, severe active bleeding, hemorrhagic shock unresponsive to IV fluids, absent or diminished peripheral pulse, bruit or thrill in the area of injury, massive hemoptysis or hematemesis, air bubbling through the wound or airway compromise, mandates urgent operative intervention,^{2,3,5,9,17,29,36,37,64} and airway control. Neurologic deficit and evolving stroke have also been considered to be hard signs of injury.^5,36

In the hemodynamically stable patient without airway compromise who has “soft” signs of injury further diagnostic evaluation of the aerodigestive tract, the vasculature, and the nervous system can be undertaken.^2,3 Patients with “no signs” of injury other than the SW or GSW, and who are asymptomatic can be observed for a minimum of 24 hours.² Observation for 24 to 48 hours^11,30,52 and serial examination every 6 to 8 hours during the period of observation has been recommended.⁵²

“Soft signs” which are suspicious for but not diagnostic of vascular injury include small to moderate sized non-pulsatile and non-expanding hematomas, minor bleeding or pulsatile bleeding that has stopped, mild hypotension that has responded to fluid resuscitation, and proximity wounds.^2,5,17,52 Some authors have considered a radial pulse deficit, and the presence of a bruit or thrill³⁶ or altered neurological status³⁰ to be soft signs.

Air embolism is possible in the presence of venous injury.³ Abrupt onset of a stroke type syndrome may herald vascular interruption, injury-induced thrombosis, or traumatic carotid or vertebral arterial dissection. After PNI the incidence of venous injury has been reported to be higher (18%–20%) than arterial injury (12%–13%).⁶⁵ However, carotid injury has also been reported to occur in 4% to 15% of PNIs and may account for 20% to 80% of all cervical vascular injuries.¹⁷ The reported mortality after penetrating carotid artery injury has been reported to be as high as 66%.¹⁷ Approximately 3% of patients with soft signs of vascular injury require a therapeutic operation.¹⁷ Physical examination alone has been reported to be a reliable indicator of clinically significant vascular injury.^{2,9,17,30,53,64,66,67} In a retrospective review, Jarvik et al.⁶⁷ found no statistically significant difference between the sensitivities of clinical examination and angiography. In a review of 145 cases of PNI, Sekharan et al.⁶⁸ found that of the 114 patients without hard signs of vascular injury, only one required operative repair. Azuaje et al.⁶⁹ reported that physical examination alone had a 93% sensitivity and 97% negative predictive value (NPV) for vascular injury in a series of 216 patients. Similarly, Demetriades et al.¹⁰ reported that none of 160 patients without clinical signs of vascular injury had serious vascular injury that required treatment. Thoma et al.¹³ concluded that the absence of clinical signs and symptoms reasonably excluded vascular injury in their series of 203 patients. Conversely, in a prospective study of 59 patients with a GSW to the neck, Mohammed et al.⁷⁰ found physical examination alone to have a sensitivity of 57%, a specificity of 53%, a positive predictive value (PPV) of 43%, and an NPV of 67%. Ten patients without clinical signs of vascular injury in fact had vascular injury.⁷⁰ The severity of the injuries identified was not defined.

In a series of 453 PNIs, 8.6% had hard signs of vascular or aerodigestive injury, and 89.7% of these patients had a clinically significant injury requiring intervention. The remainder had soft tissue bleeding that required extensive surgical wound care.² One hundred and eighty-nine patients (41.7%) had no signs of vascular or aerodigestive tract injury, and no injury was detected during observation and follow-up. Two hundred and twenty-five patients underwent multidetector computed tomographic angiography (MDCTA). Thirty-nine of these patients underwent MDCTA for proximity of the trajectory only, and all of these were negative. Twenty-eight injuries were detected in 22 of the 186 patients with soft signs of injury. Twenty-one of these patients required surgical or interventional radiology treatment.²

Hematoma is the most common sign of vascular injury, followed by shock and external bleeding.⁹ As mentioned above, bleeding within the compartmentalized spaces of the neck can produce insidious displacement and distortion of the airway without external evidence. Airway obstruction can occur precipitously following a period of apparent quiescence, and airway control can be difficult.²⁹ For this reason, any evidence of direct vascular injury to the neck has been said to be justification for early endotracheal intubation.²⁹

The signs and symptoms of aerodigestive injury include hoarseness or dysphonia, stridor, SC emphysema or crepitance, dyspnea, dysphagia, hemoptysis, odynophagia, hematemesis, tenderness on palpation of the larynx, and air bubbling from the wound.^3,5,9,11 Decreased breath sounds may be due to a hemothorax or pneumothorax.³ Aerodigestive tract injuries can be subdivided further into laryngotracheal and pharyngoesophageal injuries.⁵ In the setting of PNI, laryngotracheal injuries are usually readily apparent.⁵ All 15 patients in the series reported by Soliman et al.⁵ who had clinically significant injuries to the aerodigestive tract met the criteria for immediate exploration. The only “hard” clinical sign diagnostic of laryngotracheal injury is air escaping from the neck wound.^14,17 Air bubbling through the neck wound, massive hemoptysis or hematemesis, or respiratory distress/airway compromise are indications for emergency surgical exploration.^2,17,36 “Soft” signs are suspicious but not diagnostic of significant injury and include minor hemoptysis, dysphonia/hoarseness, dyspnea, agitation, and SC emphysema.^2,5,17,36 Soft signs are present in approximately 18% of PNIs and these patients require further investigation to identify significant injuries that require repair.¹⁷ Approximately 15% of patients with soft signs have a significant laryngotracheal injury.¹⁷ SC emphysema, found in 7% of patients with PNI, is the most common soft sign and may be due to laryngotracheal injury, esophageal injury, or associated pneumothorax.^5,17,36 In approximately 15% of cases, no source of the SC emphysema is found and it is presumed that the air entered through the wound.^17,36 Hoarseness is an indication of significant airway injury until proven otherwise.³⁴ Demetriades et al.¹⁴ reported that SC emphysema (clinical or radiological) was almost always present in penetrating aerodigestive tract injuries and SC crepitus was the most common finding reported by Grewal et al.³² in a series of 57 patients with penetrating laryngotracheal trauma. An absence of signs or symptoms suggestive of aerodigestive trauma has been found to reliably exclude injuries requiring surgical repair in a series of 152 patients.¹⁰ Soliman et al.⁵ reported similar findings in a series of 163 patients. Emergency airway management has been required in 46% to 56% of patients with penetrating laryngotracheal injury.^31,32,34

Pharyngoesophageal injury due to penetrating neck trauma can be occult and difficult to diagnose on physical exam. There are no hard signs diagnostic of injury.^17,36 Signs and symptoms suggestive of pharyngoesophageal injury include deep cervical pain, chest pain, dysphagia, odynophagia, hematemesis or hemoptysis, SC crepitus/emphysema, a positive sip test (pain on swallowing a sip of water), and retropharyngeal or mediastinal air on x-ray.^3,5,17,36,52 “Soft” signs including odynophagia, SC emphysema, hematemesis or hemoptysis are present in approximately 23% of patients with PNI and require evaluation, but only 18% of patients with these findings have pharyngoesophageal injury.¹⁷ In the complete absence of these soft signs, it is highly unlikely that the patient has an injury requiring treatment.¹⁷

A thorough neurologic evaluation is necessary to detect or rule out penetrating injury to the central nervous system, cranial nerves, or peripheral nerves.³ Complete spinal cord transaction above C5 can lead to respiratory arrest, and injury below C5 can cause respiratory distress.³ Injury to cranial nerve (CN) VII is manifested by facial weakness, CN XI by an inability to shrug the shoulders, and injury to CN XII by deviation of the tongue.³ Injury to cervical nerve roots C5-C7 will manifest as sensory and motor deficit to the ipsilateral extremity.² Interruption of carotid or vertebral arterial flow can cause ischemic stroke.³ The identification of unstable cervical spine and spinal cord injury associated with PNI is important as immobilization has implications for airway management as well as physical examination.

It has been recommended that all patients with PNI be immobilized in a rigid cervical collar,⁷¹ despite the fact that unstable cervical spine injury in PNI due to SWs is exceedingly rare. In the retrospective study by Rhee et al.,⁷² of 7483 patients with SWs, nine had cervical spine fracture, of whom six had spinal cord injury. Two additional patients had a cervical cord injury but no fracture. Three patients required stabilization, none of whom were neurologically intact at presentation. All patients with cervical cord injury had obvious neurological deficit at the time of presentation. A GSW to the neck would need to disrupt the cervical spine in two of the three stabilizing columns to make the spine unstable and it is highly likely that the spinal cord would be injured as well in this setting.⁷² In the study by Rhee et al. cervical spine stabilization was required in 26 patients after GSW. All patients with cervical spinal cord injury due to a GSW sustained the injury at the time of the GSW, and none had significant neurologic recovery despite stabilization. Cervical spine stabilization was required in four of 12,559 patients (0.03%) with a GSW who were neurologically intact.⁷² In a study reported by Klein et al.,⁷³ 33 of 183 patients with GSWs to the neck had cervical spine injuries. However, only one of the 33 had a proven significant spinal injury with no neurologic findings on admission.⁷³ The authors concluded that immobilization is essential for patients with GSWs to the neck until radiologic evaluation is complete.⁷³ In a retrospective study by Medzon et al.,⁷⁴ 19 of 81 patients who had sustained a GSW to the head or neck had documented cervical spine fractures. However, of the 65 patients who were alert and without neurologic deficits, only three had a fracture, none of which were unstable.⁷⁴ Sixteen of the 19 patients with fractures required acute airway management. The authors were reluctant to recommend removal of collar immobilization based on their data. However, they note that the likelihood of an unstable fracture in an alert and examinable patient without neurologic deficit is low.⁷⁴ They went on to suggest that the decision to remove the collar or discontinue spinal precautions should be individualized, and when emergency airway control is required, it would be reasonable to remove obstructive devices to permit more expeditious treatment.⁷⁴ In a retrospective review of 27 patients with PNI by Connell et al.,⁷⁵ 12 patients sustained a spinal cord injury, one due to a GSW and 11 from sharp weapons. Ten patients had obvious clinical evidence of spinal cord injury and two were in traumatic cardiac arrest. The authors concluded that fully conscious patients with isolated penetrating trauma and no neurologic deficit do not require spinal immobilization.

The retrospective review performed by Lustenberger et al.⁴ included 1069 patients with PNI of whom 463 sustained a GSW and 606 a SW. A cervical spine injury was diagnosed in 65 patients (6.1%), 56 due to GSW and nine due to SW. Spinal cord injury occurred in 34 patients (3.2%), 32 in the GSW group and two in the SW group. The cervical spine injury was considered unstable in four patients (0.4%), all following GSWs and all of whom had obvious neurological deficits or altered mental status at the time of admission. There were no cases of cervical instability after cervical SW. The authors concluded based on their data that cervical spine immobilization has no role after SW to the neck. The incidence of unstable cervical spine injury after PNI is exceedingly low (0.4%) and all patients in their series had neurological deficits or altered mental status at presentation. Spinal immobilization may be of value after GSW to the neck, however, monitoring for hematoma and other life-threatening complications must take priority.⁴

Based on the available evidence, it appears unlikely that isolated PNI would produce an unstable cervical spine injury in the alert, examinable patient without a detectable neurologic deficit. Immobilization in this setting can interfere with airway management, can obscure findings on physical examination of the neck, and should only be considered when the mechanism of injury and/or physical findings suggest spinal cord involvement.⁶ The value of spinal immobilization by means of a collar in patients with PNI is questionable and may be harmful in some patients.¹⁷ A 2007 review of PNI stated that it has no role in SWs to the neck and is of limited value in GSWs to the neck.¹⁷ In the presence of coincidental blunt trauma, an altered level of consciousness, or neurologic deficit, immobilization is indicated.

The patient presented here underwent cervical spine immobilization. He had the only hard clinical sign of laryngotracheal injury on clinical examination, air escaping from the entry wound in the anterior neck. There were no signs of vascular or neurologic injury.

What Airway Management Techniques Are Appropriate in PNI?

About 8% to 10% of patients with PNIs present with airway compromise, and approximately 30% of patients with laryngotracheal injuries require emergency airway management.¹⁷ The airway compromise may be due to direct trauma, severe edema, or external compression by hematoma.¹⁷ Airway management is the first priority and can be intimidating and challenging even for the most skilled practitioners due to the coexistence of a potentially difficult airway and the need for rapid action.^1,29,76 In addition, the rarity of PNI means that the experience of any one practitioner in the management of this injury can be limited.⁷⁷ The need for airway control must be determined and the time available to achieve that control must be estimated. There must be a willingness to act quickly despite incomplete information as a delay in intervention can be hazardous,²⁹ and there must be an ability to improvise and change plans under rapidly changing circumstances.³⁴ Airway management decisions must be based on the patient’s specific injuries, existing signs of airway compromise, the anticipated clinical course and risk of deterioration, the need for transport, and the patient’s overall condition and level of cooperation, as well as planned diagnostic and therapeutic interventions.^7,29 On examination, evidence of injury to an air-containing structure in the neck (SC emphysema, stridor, dysphagia, odynophagia, respiratory distress), vascular injury (hematoma, active bleeding, shock, palpable thrill, carotid bruit, absent or diminished pulses), and spinal cord injury (motor and sensory deficit) must be evaluated. The presence of inspiratory stridor implies impending loss of the airway.⁶⁵ The likelihood of difficult direct laryngoscopy must also be assessed. Emergency airway management may be necessary to secure a patent airway, in preparation for operative intervention, or as a part of airway evaluation in selective management of PNI.⁷ Emergency airway control is indicated in the presence of airway obstruction, respiratory failure/distress, signs of significant airway injury, inability to protect the airway from aspiration, hemodynamic instability,⁷ and hard signs of vascular injury that mandate emergency surgical intervention.^6,9,37 Edema, SC emphysema, or hematoma can produce sudden airway obstruction following a period of relative quiescence, and anatomic distortion can make intubation or a surgical airway more difficult to perform.²⁹

The decision to observe a patient for impending airway compromise, or to secure the airway to avoid a difficult intubation in the presence of anatomic distortion, is a matter of clinical judgment.^29,76 This decision must be based on the evidence on clinical examination of significant vascular, aerodigestive tract, and neurologic injury, and recognize that if one chooses to “observe,” complete airway obstruction may occur suddenly and be irreversible. The airway should be reevaluated frequently.⁶⁵ If there is evidence of injury to an air-containing structure in the neck (larynx, trachea, pharynx, esophagus), positive pressure bag-mask-ventilation may be hazardous and can produce increased anatomic distortion, disruption, and airway obstruction.^3,6 Laryngeal mask airways should not be used as their efficacy is decreased in the presence of anatomic distortion and they may worsen the injury.⁷⁸ Orotracheal intubation in the presence of laryngotracheal injury risks cannulation of a false passage, further disruption of damaged mucosa, and increased airway compromise.^14,79,80 If there is evidence of significant vascular injury, airway management is indicated.²⁹ As mentioned above, a hematoma can expand in the deep tissue planes of the neck and airway compromise may proceed insidiously only to be followed by rapid and catastrophic deterioration.²⁹

The timing, place, and method of airway control depend on the type of neck injury, the cardio-respiratory condition of the patient, the available resources, and the experience and skills of the resuscitation team.^3,10,17,81

Several investigators have reported experience with airway management in PNI.

Shearer et al.⁴³ reviewed the records of 107 patients who required an artificial airway from a series of 282 patients admitted with PNI. A surgical airway was the primary choice in 6%, RSI in 83%, awake bronchoscopic intubation in 7%, and blind nasal intubation in 4%. The success rates for these various techniques were: primary surgical, 100%; RSI, 98%; awake bronchoscopic, 100%; and blind nasal, 75%. Eight of the 107 patients had laryngotracheal injuries (8%) and 38 patients had vascular injuries (35.5%). RSI failed in two patients (2%) and a surgical airway was required. One blind nasal attempt failed (25%) and was followed by loss of the airway and death during attempted cricothyrotomy. Tracheotomy was performed as the primary airway in three of the eight patients with laryngotracheal injury. Of the nine patients who were hemodynamically unstable, five underwent a tracheotomy or cricothyrotomy in the ED. The authors concluded that airway control can be achieved in most patients with a PNI by RSI or a surgical airway, and that a surgical airway should be strongly considered in patients who have wounds in proximity to the larynx who have stridor, dyspnea, hemoptysis, and SC emphysema.⁴³

Mandavia et al.⁸² conducted a retrospective study of ED intubations in patients presenting with PNI at a level I trauma unit over a 3-year period. Seven hundred and forty-eight patients with PNI were evaluated in the ED, of whom 82 (11%) required immediate airway management. Twenty-four of these 82 patients were excluded due to pre-hospital cardiac arrest or intubation. In the remaining 58 patients (45 GSWs, 12 SWs, 1 motor vehicle collision), 39 underwent RSI with a 100% success rate. Thirty-three patients required one attempt, four patients required two attempts, and two required three attempts. Oxygen desaturation (less than 90%) occurred in two patients. Five unconscious patients were intubated orally without paralysis, and two underwent emergency tracheotomy. Flexible bronchoscopic intubation was attempted by ENT residents in 12 patients and was successful in nine. The three remaining patients were successfully intubated by RSI, although one patient required two attempts and experienced oxygen desaturation to 79%. Both patients who underwent emergency tracheotomy had GSWs and were unable to phonate properly. One of these patients had a laryngeal injury confirmed by endoscopic laryngoscopy prior to tracheotomy. Oral endotracheal intubation was the definitive technique in 47 of the 58 patients and was successful 100% of the time it was employed. The authors concluded that RSI was safe and effective in all of the cases in which it was attempted, and that practitioners with airway expertise should consider using RSI in the setting of PNI.⁸²

Eggen and Jorden³⁸ reviewed the charts of 114 patients with penetrating injury that breeched the platysma. The mechanism of injury was GSW in 59, SW in 39, SGW in seven, and miscellaneous in nine patients. Sixty-nine patients required intubation, of whom 26 were intubated urgently. Urgent airway control was considered necessary in the presence of acute airway distress, airway compromise from blood or secretions, extensive SC emphysema, tracheal shift, or severe alteration of mental status. Eight of the 26 urgent intubations were initially unsuccessful, and six of these required an alternative technique. Four of these were failed oral intubation, three of whom were subsequently managed via the open wound, and one via a tracheotomy. Two of the six were failed nasotracheal intubations both of whom required emergency tracheotomy. Of the 26 patients who required urgent airway control, nine required a tracheotomy and five of these patients had diffuse SC emphysema. Of the 98 patients with zone II injury, 22% required urgent airway control whereas all three patients with zone I injury, and five of 13 (38%) with zone III injury required urgent airway control. The authors noted that a variety of approaches to airway management have been documented to be successful, and that no approach should be dismissed unless specific circumstances contraindicate it or make it technically impossible.³⁸ This study was published at a time when RSI was not widely practiced by emergency physicians.