Perspective

A person’s face is the focal point of conversation and social interaction. Within the face is embodied each person’s mode of expression and communication. The face also has a receptive importance, with many special sensory functions of the body located within the facial structures. It is not surprising that facial disfigurement harbors the potential for both physical impairment and long-term psychologic sequelae.^1,2

Death from facial trauma is rare, and the severity of facial injuries is often perceived by the patient to be out of proportion to the actual injury. The goal of the emergency physician (EP) is to secure the airway, identify the injury, preserve appearance, and consult with the appropriate surgeon to determine further treatment and follow-up.³ Although zygomatic and nasal fractures may occur in isolation, any fracture of the frontal bone and maxilla must raise suspicion for the possibility of associated facial fractures, intracranial injury, and concomitant cervical spine injury.^4–7 Proper diagnosis and recognition of zygoma and nasal pathology are essential for maintenance of adequate cosmetic and physiologic function. Trauma involving the mandible, the strongest facial bone, may result in fracture or dislocation. Fifty percent of mandibular fractures occur at two or more locations because of its pseudo-ring shape. Detection of one fracture site should always prompt a search for a second fracture.⁸

General Anatomy

The major bones of the face create the defining features and include the frontal, nasal, zygoma, maxilla, mandible, and temporal bones. The orbit consists of the maxilla, zygoma, frontal, sphenoid, orbital, and lacrimal bones (Fig. 76.1).

Fig. 76.1 Facial bones and essential structures of the facial anatomy.

The face is conventionally divided into thirds: upper, middle, and lower. The borders of each third are loosely defined by branches of the trigeminal nerve, which provides sensory innervation to the face. Identification of the exiting foramen for the distributing branches of the trigeminal nerve (cranial nerve V) is crucial when providing local nerve anesthesia (Fig. 76.2).

Fig. 76.2 Anatomic location and distribution of the trigeminal nerve.

The facial nerve (cranial nerve VII) intricately courses through the parotid duct and provides parasympathetic innervation, special sensory function to the tongue and soft palate, and general motor function to the 44 muscles of facial expression. Deep facial lacerations between the tragus and lateral canthus may jeopardize the integrity of the facial nerve. Any damage to the facial nerve distal to the stylomastoid foramen can result in facial nerve dysfunction, commonly referred to as Bell palsy.

The parotid duct lies in a plane with the tragus and inferior corner of the nasal vestibule. Competency of the parotid duct must be considered in patients with deep lacerations in this region of the face (Fig. 76.3).⁹

Fig. 76.3 Location of the parotid duct complex.

The external carotid artery is the major vascular supply to the face. This vessel provides extensive collateral supply to the midline tissues through anastomosis (Fig. 76.4).¹⁰

Fig. 76.4 Vascular supply to the face and skull.

Approach to Multitrauma Patients with Facial Injuries

The degree of tissue distortion following facial trauma should not dissuade the EP from addressing the initial treatment priorities in patients. Though uncommon, facial trauma can be a life-threatening insult, and the EP must address life-threatening injuries before evaluating the obvious facial injury. The mere presence of a facial fracture, particularly one involving the midface, greatly increases the risk for traumatic brain injury.^11,12 The energy required to fracture the midface is often transmitted to the neurocranium, and such fractures are associated with a high incidence of brain death. In general, patients with facial fractures who do not survive have higher injury severity scores and lower Glasgow Coma Scale scores and consist of an older population. Other typical concomitant injuries include pulmonary contusions, abdominal injuries, and cervical spine injuries.¹³ The emergence of motor vehicle air bags has decreased patient mortality. However, increased concern is warranted for injuries to the orbits, globes, facial soft tissues, and temporomandibular joints, as well as cervical fractures of the posterior arches of C1 and C2.

The blood supply to the face consists of a complex system involving branches of the internal and external carotid arteries with several anastomoses between them. The majority of the facial vascular supply is via the internal maxillary artery, which originates from the external carotid. The internal maxillary artery passes between the Le Fort fracture lines and can be dissected with severe midface trauma.

Treatment of bleeding must begin with inspection of the airway and maintenance of its patency. Local hemorrhage may be controlled with posterior nasal packing or insertion of a Foley catheter into the nasopharynx and inflation with air. The catheter should be gently pulled anteriorly in an attempt to close the posterior choana. Temporary external reduction of fractures may also provide stabilization of arterial injuries. Finally, surgical ligation of the external carotid artery or transcatheter arterial embolization of the maxillary artery can be performed to effect hemostasis.¹⁴ Less obvious sources of serious blood loss must be monitored (scalp lacerations, nasal fractures, mandibular fractures) because persistent bleeding may lead to hypovolemia.¹⁵

Pathophysiology

The force necessary to fracture the frontal bone is commonly the result of a motor vehicle accident in which the forehead strikes the dashboard or steering wheel. Assault with a blunt object is also a common injury mechanism.

Anatomy

The frontal bone is the only constituent of the forehead; the prominent protuberance is called the glabella. Within the frontal bone resides the frontal sinus, which communicates with the nasopharynx via the frontonasal canal. The anterior bone of the frontal sinus is thicker than the posterior aspect. The intracranial dura mater is adherent to the posterior frontal sinus wall. Cutaneous innervation of the frontal bone is supplied by the superior orbital nerve, a branch of the trigeminal nerve.

Treatment

Frontal sinus fractures are usually diagnosed by computed tomography (CT). Displaced anterior wall fractures require either immediate repair or delayed reconstruction. Conversely, frontal bone fractures that involve the posterior wall of the sinus are associated with cerebrospinal fluid (CSF) rhinorrhea; the patient will require urgent consultation with a neurosurgeon and admission to the hospital.¹⁶ Ocular trauma or sudden loss of vision associated with a frontal bone injury requires immediate ophthalmologic consultation.

Follow-up, Next Steps in Care, and Patient Education

Anterior frontal sinus fractures without any concomitant injuries are not life-threatening; the patient can be discharged with close consultant follow-up to maintain an adequate cosmetic result. Although antibiotics have not been shown to decrease the incidence of meningitis associated with a CSF leak and frontal bone fracture, antibiotic therapy should be based on the consultant’s preference.

Pathophysiology

Trauma to the eye can result from falls, motor vehicle accidents, and direct blows from an assault or a projectile object (hockey puck, baseball). Serious eye injury has been shown to most commonly be associated with midface fractures.^17,18 Ocular trauma can be divided into two broad categories: direct trauma to the globe and trauma to the orbit. Direct globe trauma ranges in severity from a benign corneal abrasion to rupture of the globe. Orbital trauma involves injuries such as benign contusions and fractures with complications to surrounding structures, including the globe and extraocular muscles.

Orbital fractures are classified as “impure” when the fracture line involves the orbital rim or as “pure” in the case of a fracture with no rim involvement. Compression of the optic nerve (ocular neuropathy) can be caused by displacement of a fracture, increased pressure from a retrobulbar hemorrhage, or optic nerve hemorrhage.¹⁹ Each of these processes has the potential to lead to rapidly progressive visual loss and is an ophthalmologic emergency.

The mechanism of orbital blowout fractures was investigated by Waterhouse et al. via the same principles as Le Fort a century earlier (see later).²⁰ Waterhouse investigated the two possible mechanisms for an orbital blowout fracture, the hydraulic and buckling theories. The hydraulic mechanism occurs when the vector of the force directed onto an uninjured globe is transmitted to the fixed orbital walls; it results in a large fracture of the inferior or medial orbital wall, or both (Fig. 76.5). This mechanism is commonly associated with herniation of the orbital contents through the fractured orbital wall, hence the term blowout. The buckling mechanism, in contrast, occurs when a traumatic force is directed to the inferior orbital rim and causes only the inferior floor of the orbit to buckle, or fracture, with no associated herniation of the orbital contents.

Fig. 76.5 Mechanism and structures involved in an orbital blowout fracture.

Herniation of the orbital contents—fatty connective tissue, inferior rectus, and inferior oblique muscles—occurs at the weakest portions of the orbit, specifically, the orbital floor and the anteromedial wall. With increased pressure on the globe, any defect in these bony structures may lead to herniation of the orbital contents and resultant muscular entrapment.

Anatomy

The globe resides within a cone-shaped socket composed of seven bones of varying thickness. The thinnest bony portion of the socket is the orbital floor. The globe is protected from trauma by the thick superior rim of the frontal bone and the inferior rim of both the maxilla and zygoma. The orbital rim possesses a smooth contour with occasional notching that is symmetric when encountered. Any asymmetric step-off of this rim is indicative of a potential rim fracture.

The eye is cushioned by a retrobulbar fat pad encasing the globe. The extraocular muscles complete the orbital anatomy by surrounding the globe and enabling eye movement. Herniation of any orbital contents through the inferior or medial walls will result in protrusion of these structures, in whole or in part, into the maxillary or ethmoidal sinus, respectively. The inferior rectus and inferior oblique muscles, both innervated by cranial nerve III, lie adjacent to the inferior and medial orbital floors and are the most commonly affected extraocular muscles with a blowout injury.

Presenting Signs and Symptoms

Patients with a history of facial trauma should undergo complete evaluation of the eye and the encasing orbit. Initial inspection may reveal periorbital ecchymosis and edema, discrepancy in eye level, or enophthalmos. Enophthalmos is consistent with an orbital blowout fracture. Anesthesia of the ipsilateral cheek and upper lip is indicative of inferior orbital nerve impingement.

Key points in the patient’s history include the following:

The eye examination should begin with palpation of the orbital rims. The rims should be evaluated for crepitus, a step-off deformity, subcutaneous emphysema, and decreased sensation in the distribution of the inferior and superior orbital nerves.

Pupil size, shape, and light reflex must be examined to assess optic nerve status. Full ocular muscle function is evaluated by slow, directed passive range of motion. Upward gaze palsy with vertical diplopia is consistent with dysfunction of the inferior rectus muscle and suggests entrapment from an orbital blowout fracture. Enophthalmos is common when a large amount of tissue herniates through an orbital floor defect into the adjacent maxillary sinus.

The EP must evaluate both eyes for visual acuity. This examination may be facilitated by using a Snellen eye chart or pocket card or by asking the patient to read the text of a newspaper or other print. Visual impairment should prompt immediate consultation for the suspected injury. If the patient’s injury allows proper positioning and cooperation, a slit-lamp examination is warranted to fully evaluate the conjunctiva, lens, iris, sclera, cornea, and anterior chamber of the globe. Intraocular pressure can be measured. However, if the globe has possibly been ruptured, intraocular pressure assessment should be deferred to an ophthalmologist.

Diagnostic Criteria and Testing

If the pretest probability of orbital or ocular damage is low or if CT is not available, a Waters view radiograph of the midface is a screening tool for fracture or resultant blood in the sinus, subcutaneous emphysema, depression of the bony fragments, or the “hanging teardrop” sign whereby herniated globe structures may be visualized in the maxillary sinus roof. If suspicion of orbital or ocular injury is high, particularly when concomitant intracranial or facial injuries are suspected, CT is required to elucidate the extent of the identified injury. This examination should include views of the head, as well as axial and coronal cuts of the midface and orbits.

Treatment

Management of blowout fractures is complicated.²¹ The presence of an orbital fracture with findings of herniation on clinical or radiographic examination requires immediate surgical consultation to guide the treatment plan. Immediate indications for surgical intervention include muscular entrapment with gaze restriction or acute enophthalmos. Contraindications to surgery include globe rupture, hyphema, and retinal tears. These injuries should prompt emergency ophthalmologic consultation. An ophthalmologist should also be contacted for patients with evidence of lens dislocation, laceration of the cornea or sclera, or rapid loss of visual acuity.

Patients with an isolated blowout fracture may be discharged home with follow-up arranged within 2 weeks to assess for resolution of the swelling. If entrapment is present at follow-up, the patient would require open reduction of the fracture. Even patients with a blowout fracture may have their symptoms improve over a 10-day to 2-week period and may not require surgical intervention.

An increase in retrobulbar pressure from a hematoma or emphysema can lead to acute and permanent loss of vision. Lateral canthotomy can be a vision-saving intervention in this context. This simple procedure is intended to relieve pressure on the optic nerve and, ultimately, preserve the patient’s vision through resolution of the optic nerve traction and ischemia. Immediate ophthalmologic consultation should be obtained to perform the lateral canthotomy; when a consultant is unavailable or if a lengthy response time is anticipated, the procedure should be undertaken by the EP.

Local anesthetic without epinephrine is injected into the lateral canthus. An incision is made in the canthus with a pair of fine, sharp scissors. The incision is made in the canthus at the juncture of the upper and lower eyelids between the globe and the orbital rim. Expulsion and drainage of the hematoma should ensue through the incision site.

Follow-up, Next Steps in Care, and Patient Education