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avoided by preemptive denitive airway control, when signs and symptoms of cervical penetrating trauma are present. The importance of reevaluation of the airway throughout the initial evaluation cannot be understated, as progression of hemorrhage or airway injury can quickly transform an ini­tially patent airway to a life-threatening airway obstruction.

This section will address the scope of penetrating injuries by anatomic location. Common injury patterns, key physical examination ndings, diagnostic adjuncts to the secondary survey, and basic tenets of therapy will be discussed.

Civilian penetrating head injuries are most commonly the result of low-velocity gunshot wounds and are frequently due to suicide attempts. In the United States, rearms are the leading mechanism of traumatic brain injury (TBI) mortality, particularly among young persons, but even in the elderly, death from self-inicted TBI ranks third after that due to TBI from motor vehicle crashes and falls. The predominant injury from projectiles is facilitated through the velocity of the object, as the energy conveyed to the tissue is proportional to the square of velocity. Injury occurs via three different mech­anisms. The direct disruption of the missile tract lacerates parenchyma and blood vessels. Shock waves produce pres­sure gradients that impact neural tissue and function beyond the path of the missile tract. Cavitation facilitates further direct tissue damage and increased intracranial pressure (ICP). For this reason, military injuries from high-velocity projectiles are usually associated with a higher rate of death that is caused by civilian weapons. It has been observed that the majority of soldiers that present for medical attention with penetrating head injuries sustains low-velocity shrapnel or shell wounds.

Computed tomographic (CT) scans of the brain and cervi­cal spine facilitate evaluation of the tract of the penetrating object, missile debris, and the secondary effects of the pro­jectiles including cerebral edema, hemorrhage, and bone fragmentation. Computed tomographic angiography (CTA) has largely supplanted cerebral angiography and should be employed liberally to evaluate for carotid and vertebral arte­rial injuries when injuries involve the sphenoid and temporal bones and posterior fossa. Early and rapid identication of vascular injury by screening CTA can allow planning for angiographic embolization or stenting of pseudoaneurysms. The limitations of CTA, with a sensitivity as low as 80% in some studies due to shrapnel artifact, should be recognized and targeted evaluation of potential injuries supplemented with subsequent duplex ultrasound or angiography.

Although increased ICP is associated with higher mortal­ity in penetrating brain injury (PBI) patients, there is little published data on the use of ICP monitoring in this patient population, primarily focused on the directed evacuation of hematoma or relief of intractable cerebral swelling. In the absence of guidelines, it is generally accepted that ICP moni­tors may be employed to follow ICPs for evidence of deterio­ration when neurologic examination is not possible, as is the practice in blunt head injury. Harvey Cushing’s experience during World War I established the standard for early and meticulous debridement of penetrating head wounds. The subsequent military experience of World War II and the Vietnam War largely supported the aggressive operative

are no prospective clinical trials of hematoma evacuation in this patient population, so this remains a class III recommen­dation. Finally, due to an elevated risk of posttraumatic epi­lepsy after penetrating brain injury to the cerebral cortex, prophylactic anticonvulsant therapy is recommended for the rst week following injury.

There is no universal approach to the diagnosis and clas­sication of penetrating facial trauma, but several authors have described schema to identify the location of the external wound and predict underlying structures at risk. The original designation of three zones of the face included everything below the hairline to the superior orbital rim (area 1), the midface from the superior orbital rim to the upper lip extend­ing laterally to the preauricular area (area 2), and the lower face from the upper lip to the hyoid bone (area 3). The use of this system directed further diagnosis and management of injuries based on the identiable injuries on screening physi­cal examination. Additionally, particular attention was paid to the injuries posterior to the angle of the mandible, as this location was associated with a higher incidence of vascular injury due to the proximity of the carotid artery and jugular vein, but these are really zone III neck injuries (see Sect.

29.2.3). This approach has been generally supplanted by a

more simple two-area designation of the midface and man­dible; this is largely due to the fact that signicant area I injuries are intracranial and not truly facial injuries, as well as to avoid the confusion due to the nomenclature and over­lap with the previously named three zones of the neck. In the newer designation, the midface includes the area from the supraorbital rim superiorly to the oral commissure inferiorly to the external auditory meatus laterally, and the mandible designates the area below the oral commissure, but not including zone III of the neck.

The mechanism of injury also bears importance in the evaluation. In general, the degree of soft tissue loss and over­all structural disruption is greater in ballistic injuries than that seen in stabbings, and knife lacerations to vascular struc­tures or nerves may be amenable to primary repair. Gunshot and close-range shotgun blasts are commonly associated with fractures and tissue loss due to their substantial kinetic energy and may leave behind signicant shrapnel and bony fragmentation. Shotgun injuries are more commonly spread across multiple areas and have a high incidence of globe injury. Although low velocity, objects such as knives have unpredictable depth of penetration. If the stab wound imple­ment is still present in the wound at the time of evaluation, it should remain in situ until after any diagnostic studies are performed and the patient is in the operating room. Vascular control can be temporarily obtained endovascularly either before or in conjunction with the operative exposure.

and involvement of the sinuses, multidisciplinary evaluation and coordinated treatment by craniofacial reconstructive spe­cialists are recommended to obtain the best long-term cos­metic and functional outcomes. Special attention should be paid to meticulous realignment of the eyelids, nasal alar rims, auricular helical rims, and oral stoma. Patients who present with obvious facial paralysis should be assumed to have sus­tained direct injury to one or more branches of the facial nerve. If the wound is posterior to the lateral canthus, a local exploration with primary nerve repair is considered the treat­ment of choice. In cases of blast trauma, the nerve is debrided beyond the visible injury, and nerve grafting should be strongly considered. Delayed onset of paralysis suggests post-injury nerve edema that may resolve without interven­tion. The parotid duct is commonly injured in association with buccal branch of the facial nerve injuries due to the prox­imity of these structures. Additional signs of parotid injury include clear uid draining from a cheek wound or sialocele formation. As the parotid duct rarely heals or recanalizes without intervention, repair over a stent is recommended.

After establishing that the airway is not at risk, maxillofa­cial bony trauma does not generally pose an immediate threat to life. As such, delayed reconstruction up to 2weeks after injury is an acceptable approach. At that time, post-injury edema has largely resolved, and the reconstructive effort may be more straightforward. In cases of severe wound contami­nation or tissue loss, multiple-staged debridements and serial dressing changes may be required to prepare the recipient bed for grafting or implantation of prosthetic material. Prophylactic antibiotics with activity against oropharyngeal ora are commonly employed, especially when there is com­munication to the sinuses for fear of development of meningi­tis. Interestingly, several reports of patients with facial fractures and cerebrospinal uid leak do not support this practice. Perioperative antibiotics at the time of facial fracture xation are associated with a signicant reduction in the inci­dence of surgical site infection. However, prolonged adminis­tration beyond 24h does not confer additional protection in contaminated head and neck surgery and may be associated with higher incidence of infectious complications. While severe facial trauma with involvement of multiple facial thirds is an independent predictor of head and neck infection, pro­longed antibiotic course (>24 h) in these patients was not associated with decreased rates of infection. While evidence tailored to patients with severe facial trauma (heavily con­taminated, multiple open fractures, etc.) is lacking, develop­ing literature questions the utility of prolonged antibiotic administration even in this high-risk patient population. As foreign bodies and necrotic, contaminated tissue serve as a nidus for infection, early debridement and extraction of bul­lets, shrapnel, and debris are indicated. This is especially true for bullets as projectiles carry clothing and other debris along the projectile track. While knives and other sharp implements

laryngoscopy and exible or rigid bronchoscopy may be undertaken in the operating room, with subsequent tracheos­tomy placement if indicated.

Ongoing evaluation continues in accordance with the Advanced Trauma Life Support (ATLS) guidelines. Along with denitive airway management, the initial management of penetrating neck injury includes an assessment of the overall stability of the patient and consideration for any other major life-threatening injuries. Chest and lateral cervical spine X-rays are helpful to rule out adjacent intrathoracic hemorrhage and spinal cord injury as alternative causes of hypotension. Any suspected concomitant pathology, such as tension pneumothorax or traumatic hemothorax, should be addressed and intervened on at this time. Active hemorrhage is controlled with direct pressure or focused balloon tampon­ade, with particular attention given to any hard signs of vas­cular injury which would indicate mandatory neck exploration (Table 29.3). While recent papers have ques­tioned the necessity of neck exploration in the hemodynami­cally stable patient with hard signs of vascular injury, these studies are retrospective in nature with inherent limitations. Observation of hemodynamically stable patients with hard signs of vascular injury is widely debated and generally not accepted as the gold standard of trauma management at this time.