Traumatic Skull and Facial Fractures

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Chapter 22 Traumatic Skull and Facial Fractures

Fred H. Geisler, Eduardo Rodriguez, Paul N. Manson

Clinical Pearls

• Linear skull fractures do not require stabilization or treatment when the scalp is closed. Depressed skull fractures may need exploration depending on the extent of the injury to the underlying brain, frontal sinus, or facial bones. Closed depressed fractures are usually repaired for cosmetic reasons. Compound depressed skull fractures with brain involvement are often neurosurgical emergencies. It becomes an emergency to treat the underlying brain injury, perform a watertight closure of the dura, and débride the devitalized scalp.

• Growing skull fractures, although rare, occur in children under 2 to 3 years of age and require surgical repair. If there is a tear in the dura accompanying a skull fracture after trauma, the pressure of the brain pulsations in a growing brain may enlarge the fracture and dural opening. The brain can herniate through this skull defect, causing a pulsatile mass under the scalp.

• Basilar skull fractures may present with periorbital ecchymoses, hemotympanum, or ecchymosis over the mastoid. The management of these fractures is usually conservative unless a cerebrospinal fluid (CSF) leak is present. Many traumatic CSF leaks will spontaneously resolve in a week. Those that do not may be managed by CSF drainage, or in some cases surgical repair to avoid infection, once the location of the leak is identified.

• Frontal sinus fractures can be diagnosed on computed tomography (CT) and are managed differently depending on whether the frontal or posterior wall is disrupted. Orbital fractures are managed based on the extent of the injury to the globe, optic nerve, and orbital contents. Patients with a fluctuating or worsening visual acuity will require decompression of their optic nerve and relief of globe pressure. There are two indications for surgery of orbital “blow-out” fractures: (1) muscle or ligament entrapment with diplopia or (2) enophthalmus (backward dislocation of the globe) caused by prolapse of the orbital contents through the fracture. Le Fort fractures are often injuries to the entire midface region. Their surgical management depends on the extent and stability of the maxillary fracture.

Skull Fractures

Skull fractures are classified in three ways: by pattern (linear, comminuted, depressed), by anatomical location (vault convexity, base), and by skin integrity (open, closed). The pattern of a skull fracture is affected by two factors. The first factor is the force of impact. A linear fracture results first at a point of weakness when the skull structure fails to undergo further elastic deformation as a response to impact; the fracture typically starts at the point of weakness in response to the maximal stress (the point of weakness is often remote from the actual impact point) and then extends to the point of impact. A comminuted fracture results when the impact force is sufficient to break the bone into multiple pieces under the point of impact and further through areas of weakness. Comminution absorbs the force of the injury. With even larger impact energies, the comminuted pieces can be driven inward to create a depressed fracture and may penetrate the dura and cortical surface of the brain.

The second factor is the ratio of the impact force to the impact area. If the impact, even one of high energy, is dispersed over a large area, as in a blunt head injury to an individual wearing a motorcycle helmet, it often produces no skull fracture, even though the brain may be severely injured. Parenthetically, it should be noted that some helmets, by the efficiency of their very force-transferring protection, have created basal skull fractures by transferred energy absorbed from protection of the vault and face and then transmitted through the mandible via the chin strap to the skull base. However, if the impact, even one of low energy, is concentrated in a small area, such as from a hammer blow, it often produces a small depressed fracture with multiple linear skull fractures radiating from the site of impact.

The location of a skull fracture is classified by its geography in two distinct areas: the skull convexity (generally termed skull vault fracture) or the base of the skull (generally termed basilar fracture). Any of the two areas can occur singly or in combination. The pattern may also become more comminuted with increasing energy forces. A skull fracture can be further classified as “open” or “closed” by the presence or absence, respectively, of an overlying scalp laceration. In addition, a fracture extending into the skull base with violation of the paranasal sinuses, the nose, middle ear, or mastoid structures is also considered an “open” fracture.

Linear Skull Fractures

A linear skull fracture is a single fracture line that goes through the entire thickness of the skull.

Diagnosis

Although it is generally accepted that clinical indications for radiological examination include loss of consciousness, retrograde amnesia, discharge from nose or ear, drainage from eardrum, dislocation of the middle ear structure or hemotympanum, positive Babinski reflex, or cranial nerve abnormalities, controversy exists (based on a cost-benefit analysis) regarding the use of plain x-rays to diagnose linear skull fractures. The patient’s eventual neurological outcome depends largely on the brain injury, rather than on the presence of a skull fracture per se. However, for a few patients radiological examination may make a crucial difference. For example, a linear fracture crossing the path of the middle meningeal artery in even a mild head injury indicates risk for late neurological deterioration from an epidural hematoma. Furthermore, computed tomography (CT) scans of the skull may detect depressed fractures, puncture wounds, and intracranial foreign objects that might otherwise elude physical examination. In practice a CT scan should be obtained in most cases; however, plain skull radiographs usually add little information. Medicolegally, it is usually best to obtain a CT scan, especially if the patient has an equivocal history or if there is evidence of a cognitive issue or indication of a significant force of injury.

Management

Linear skull fractures require no stabilization or exploration when the scalp is closed, and when there is no evidence of epidural hematoma or underlying dural or cortical injury. Even when a scalp laceration is present, very seldom is surgical exploration with bone removal necessary. Exceptions would include a machete injury to the skull producing a linear skull fracture with underlying dural laceration and brain damage. The skull fracture does, however, show that significant head trauma has occurred, and a careful assessment of the brain, facial structures, and cervical spine is required. Open linear fractures are débride of foreign material, devitalized soft tissue, and bone fragments; preferably, the damaged soft tissue at the edges of the laceration is excised to healthy, noncontused bleeding tissue (if the tissue excision can be tolerated and will permit primary closure) and the laceration is closed after thorough cleansing. If there is insufficient vascularized soft tissue present to permit excision of the contused devitalized tissue, a rotation flap and skin graft to the donor area may have to be considered (Fig. 22.1).

FIGURE 22.1 Open skull fracture (A) with tissue loss (B) sufficient that an immediate (C) scalp rotation flap had to be performed to achieve scalp closure.

Growing Skull Fractures in Children

A rare complication after linear skull fracture in young children (usually younger than 2 or 3 years) is a “growing” skull defect at the fracture site. In these cases, the dura is torn under the linear skull fracture. The pathogenesis is thought to be an expanding pouch of arachnoid passing through the torn dura and skull fracture, acting as a one-way valve that traps cerebrospinal fluid (CSF) and causes progressive pressure erosion of the fractured edges to enlarge the fracture. Alternatively, the growth of the brain, which produces pulsating, spreading tensile pressure forces on the edges of an unrepaired dural laceration, may also cause a skull defect to enlarge. These vectors of force by the brain may sometimes cause herniation through the skull defect, causing a new neurological deficit (Fig. 22.2). These lesions are surgically repaired with closure of the dura or with a dural patch and replacement or repair of the bone defect. Some surgeons routinely take a skull film at 1 year after linear skull fracture treated nonoperatively to detect such growing skull fractures. For this reason it is worthwhile for the primary care doctor to examine the scalp and skull of any child with a known skull fracture under the age of 2 or 3.

FIGURE 22.2 “Growing”” skull fracture in a child. The mechanism is a closed skull fracture that tears the dura. The pressure of the pulsating brain creates slow erosion of the bone, creating a bone and dural defect. Repair of the dura and cranioplasty is required.

Comminuted Fractures

A comminuted fracture occurs when multiple linear fractures radiate from the point of impact. Some of the fracture lines may involve the suture lines (diastatic fracture) or may stop at them. Around the point of impact there may be free fragments of bone.

Diagnosis

Diagnosis is made on skull radiographs and CT of the head with bone windows.

Management

If the skin is closed, and no depression of bone fragments greater than the thickness of the skull is demonstrated on CT, management is as that for linear skull fractures. However, in many of these cases, surgery is performed for the underlying intracranial injury, such as an epidural hematoma (Fig. 22.3). After the intracranial injury has been corrected, the bone fragments are primarily replaced as a bone cranioplasty after cleaning.

FIGURE 22.3 Comminuted minimally depressed open skull fracture with underlying epidural hematoma. A, Computed tomography (CT) scan through the center of the depressed region. Note the small amount of air at the anterior edge of the epidural hematoma. B, Intraoperative view of the depressed bone before evaluation. C, The bone was removed, sutured together, and replaced as a cranioplasty. The epidural hematoma was removed after the bone fragments had been removed.

Missing bone can be replaced with a titanium mesh screen. If the skin is open, and free bone fragments are present, cleansing or débridement of the contaminated fragments is performed, before dural and scalp closure (Fig. 22.4). Bone too contaminated may be discarded, and a titanium screen is then used to span the bone defect (Fig. 22.5).

FIGURE 22.4 Comminuted skull fracture involving a diastatic fracture of both coronal sutures and additional fractures of the frontal and parietal bone bilaterally. In this case, the skin was open and cerebrospinal fluid was coming from the wound. A, Lateral radiograph demonstrating the comminuted fracture. B, Computed tomography scan with bone windows near the top of the head showing the comminuted fracture.

FIGURE 22.5 A titanium screen can be used to span a bone defect when autologous bone cannot be used because it is contaminated and must be discarded.

Depressed Skull Fractures

In a depressed skull fracture, the greatest bone depression can occur at the interface of fracture and intact skull or near the center of the fracture if several fragments are displaced inward. Impacted fractures may be “wedged” into position by blocked bone edges.

Diagnosis

Some patients with depressed skull fractures experience initial loss of consciousness and neurological damage owing to the force transferred from the impact through the skull and into the brain. However, 25% of patients experience neither loss of consciousness nor neurological deficit. Another 25% of patients experience only brief loss of consciousness. Although the diagnosis of a depressed skull fracture is often indicated on routine skull radiographs by an area of double density (overlying bone fragments) or by multiple or circular fractures, the full extent and depth of injury are rarely appreciated with a CT scan. Physical examination is more difficult in the presence of scalp mobility and swelling. Scalp mobility can result in nonalignment of the sheared layers of the scalp or a scalp laceration and can therefore simulate, under palpation, the sense of a skull fracture; normal skull under a scalp laceration also does not exclude a depressed fracture 1 or 2 cm from one edge of the laceration. Furthermore, post-traumatic swelling of the scalp minimizes the palpable and visual appearance of the step-off at the bony edges, preventing accurate clinical assessment of the extent of a skull deformity or displacement for the first few days.

CT is the diagnostic method of choice. When image display windows are adjusted to optimize bony detail, they display the position, extent, and number of fractures as well as the presence and depth of depression. With the imaging windows set to optimize intracranial contents, the same CT scan also allows assessment of the underlying brain for contusion or hematoma, small bone fragments, or foreign bodies as well as other intracranial trauma. Occasionally, coronal CT images through fractures near the vertex of the head or extending into the skull base are used to supplement the standard CT images, because the depth of a depression is more accurately measured on CT images perpendicular to the depression.

Management

Combined therapy of depressed fractures of the cranial vault extending to involve the frontal sinus or facial bones is covered in the sections on facial fractures. When a depressed skull fracture on the convexity also includes facial fractures, the intracranial injury is typically repaired first with removal of intracerebral hematoma and repair of dural laceration if present (Figs. 22.6 and 22.7).

FIGURE 22.6 Open frontal and facial fracture. A, View of frontal skull fracture under the wound. B, Computed tomography scan showing the epidural hematoma under this open skull fracture.

FIGURE 22.7 Open dressed skull fracture involving the frontal bone with extensive fractures and displacement of bones of the orbit and ethmoid region. A, Presenting scalp laceration. B, Computed tomography scan at the level of the orbit demonstrating extensive orbital and ethmoid fractures with displacement of the bony facial structures.

Although a focal neurological deficit from the cortex directly under a depressed skull fracture is occasionally improved by elevation of the bone fragments (presumably by increasing local cortical blood flow), elevation usually produces no neurological change, implying that the initial impact produces the major cortical damage responsible for the brain deficit. The brain dysfunction usually undergoes a neurological recovery phase of several weeks to months, similar to that after a stroke or head injury without a depressed fracture. Likewise, the incidence of epilepsy after a depressed skull fracture is determined by the cortical damage at the time of impact. Therefore, the treatment of depressed skull fractures is based on relieving pressure on the brain (initiating neurological recovery), minimizing epilepsy, correcting cosmetic deformity, and preventing infection.

In closed, depressed fractures, the major indication for surgery is usually cosmetic, with the procedure performed on an elective basis in the first few days after the trauma, once the patient is cleared for elective anesthesia. The greatest cosmetic deformity occurs in the forehead. Exploration is more urgent for a large, closed depressed fracture when the radiological appearance suggests dural laceration, brain penetration, simultaneous frontal sinus fracture, mass effect, or underlying hematoma. The hematoma is evacuated, the dura is repaired, and the bone fragments are replaced and held in position with small plates and screws.

A compound depressed fracture is a neurosurgical emergency because of the risk of bacterial infection of the cranial cavity. The initial surgery is performed within 24 hours and usually within the first 12 hours. The major objectives are removal of contaminated bone fragment and foreign material; débridement of devitalized scalp, dura, and brain; and provision of a watertight closure of the dura. Often, foreign material or hair wedged between bone fragments cannot be seen through the overlying scalp incision, so simple irrigation and closure may be inadequate for débridement of foreign material. Dural closure is essential to prevent CSF leaks from the wound and brain herniation into the fracture area. Dural closure is essential to prevent CSF leaks from the wound and brain herniation into the fracture area. Dural closure also presents intracranial spread of infection from a scalp wound. Reconstruction of the calvarium is performed during the initial surgery if considered safe: otherwise a cranial defect is left and the cosmetic repair is performed later. The major reasons to consider deferred calvarial reconstruction are to shorten additional anesthesia and blood loss by major head injury or multitrauma, especially with hemorrhage; gross contamination of wounds where the bone fragments cannot be adequately cleaned; and a delay of more than 24 hours for the initial surgery.

The scalp laceration associated with a compound depressed skull fracture is usually stellate and may contain areas of contused/devitalized tissue. These areas require débridement to normal vascularized scalp to allow prompt healing and prevent breakdown of the partially viable scalp covering the fracture site (see Fig. 22.1). Scalp breakdown can many times be treated locally but occasionally will require early flap coverage. If early flap coverage is not successful, the replaced cranial bone may require débridement of any dead or nonviable necrotic bone or portion of the skin flap; a subsequent flap rotation and delayed cranioplasty will be required in stages.

Depressed Fractures over Dural Sinuses

Depressed skull fractures over a venous sinus require special handling. Surgical elevation of these fractures may involve massive blood loss if a depressed fragment has been plugging a sinus tear. There are two strategies for management. The fracture can be carefully elevated, attempting to gain control of the venous sinus as soon as possible, preparing for significant transfusion requirements. If the fracture site is not grossly contaminated with foreign material, or will not cause a major cosmetic or functional deformity, or not cause intracranial hypertension secondary to sinus occlusion, such fractures are managed with scalp débridement alone and irrigation, followed by serial CT scans for signs of brain abscess for at least a year. A delayed cranioplasty may then be required for contour. The management of these fractures requires both judgment and experience as no definite rules apply to the variation of presentations.

Basilar Skull Fractures

Fractures of the base of the skull occur in 3.5% to 24% of head-injured patients. This wide variation results from differences in study populations and the difficulty in obtaining radiographic verification of the fractures. Linear fractures in the skull base carry a risk of meningitis, whereas this risk is extremely low in fractures of the convexity unless the scalp, bone, and dura are all violated. The dura is easily torn in a basal skull fracture; this places the subarachnoid space in direct contact with the paranasal sinuses or middle ear structures, providing a pathway for infection. For example, a persistent fistula allows a continuous CSF leak, and bacterial colonization of the meninges will eventually develop.

Petrous bone fractures can either be either longitudinal or transverse, relative to the long axis of the petrous pyramid. Longitudinal fractures are more common and usually involve the tympanic membrane or external ear canal, thereby producing otorrhea. Transverse fractures result from higher-energy impacts and can damage middle ear ossicles or the facial nerve. These fractures occur with or in continuity with linear, comminuted, or depressed skull fractures and not infrequently are large linear extensions of vault fractures, crossing the base of the anterior and middle cranial fossae (Fig. 22.8).

FIGURE 22.8 Type III frontobasilar fracture involves both the lateral and the central segments of the anterior skull.

Clinical signs of basal skull fractures include bilateral periorbital ecchymoses (spectacle hematoma) (Fig. 22.9), anosmia, or CSF rhinorrhea for anterior skull base fractures, as well as hemotympanum, blood in the external auditory canal, seventh or eighth cranial nerve palsies, ecchymoses over the mastoids (Battle’s sign), or CSF otorrhea for temporal bone fractures (Fig. 22.10). Frequently, the CSF leak is first detected several days or weeks after the trauma. This delay often occurs because the CSF leak was hidden in bloody nasal discharge from facial fractures, or less frequently, it is the result of delayed development of hydrocephalus with rupture of the arachnoid at the fracture site. A larger clear ring surrounding a central blood-tinged clot when a few drops of bloody discharge are placed on a paper towel indicates that CSF is probably mixed with the blood. This sign (the “double ring”) can also be noted on the patient’s pillow during rounds.

FIGURE 22.9 Bilateral spectacle hematoma from an open frontal sinus anterior skull base fracture.

FIGURE 22.10 Cerebrospinal fluid leaks from the ear canal and a hematoma is visible in the postauricular area. These are signs of a fracture at the junction of the middle and posterior cranial fossa.

Basal skull fracture with CSF rhinorrhea is common after head injury and has an estimated incidence in the United States of 150,000 cases per year. A clear, watery nasal discharge containing glucose indicates CSF rhinorrhea. An intermittent CSF leak from the paranasal sinuses can often be demonstrated by having the patient sit on the edge of the bed with the head close to the knees for 2 minutes and watching for clear fluid to drip from the nose. CSF mixed with blood may form a halo on a piece of gauze it touches. Testing for beta-2 transferrin presence in the fluid confirms the protein found almost uniquely in CSF.

Management

Basal skull fractures are managed depending on whether a CSF leak is present. A patient with a basal skull fracture but no leak is observed for 2 to 3 days. During this time, repeated checks for rhinorrhea and otorrhea are made to verify the absence of a CSF leak. Otorrhea is more likely than rhinorrhea to resolve spontaneously. Because antibiotics are not effective in preventing meningitis over a prolonged interval and select for resistant organisms if an infection occurs, “prophylactic” antibiotics are not used on a prolonged basis in patients with basal skull fractures. When definitive closure of a leak is performed, perioperative antibiotics are utilized.

A CSF leak is managed initially by observing the amount of leakage and monitoring for signs of infection: change in temperature, altered mental status, or increased white blood cell count. Radiographic or imaging studies may indicate the area and size of the defect, which may suggest the likelihood of spontaneous closure. Most traumatic CSF leaks resolve spontaneously within the first week. If the leak persists beyond 5 to 7 days, lumbar punctures are performed daily for 3 days, removing 30 to 50 mL of spinal fluid each time, attempting to decrease the CSF pressure.

If spinal taps fail to stop the leak, spinal drainage can be used for 72 hours with the patient in a 30-degree head-up position. Should pneumocephalus develop during the course of the CSF drainage, the drainage procedure is terminated and the dural leak is surgically closed. CSF leaks refractory to spinal fluid drainage require surgical closure; the exact site of the leak is determined preoperatively from a CT scan with water-soluble intrathecal contrast or from a nuclear cisternogram with nasal pledgets for small or questionable leaks. A CT scan of the base of the skull can provide additional details of the pattern and size of the bone spicules in the fracture.

CSF otorrhea usually occurs through a fracture in the petrous bone with perforation of the tympanic membrane, although it can occasionally take place through a laceration of the external canal via fractured mastoid air cells. If the tympanic membrane remains intact, CSF that has gained access to the middle ear can flow through the eustachian tube and present as rhinorrhea. In these cases, the CT scan typically images a fracture in the temporal bone and fluid in the mastoid air cells and middle ear. Blood from the ear canal or a tympanic canal laceration may also be caused by a temporomandibular joint injury or dislocation, either of which may produce some of the same symptoms (bloody fluid from the ear canal).

A patient with CSF otorrhea often presents with hearing loss from blood in the external ear canal. Irrigation and probing of the ear in cases of suspected otorrhea are not indicated initially because they increase the risk of infection. Such a patient is managed by placing a loose-fitting sterile gauze pad over the ear; the pad is changed every nursing shift and saved as an indicator of the amount of drainage from the ear. Most cases of otorrhea stop spontaneously within the first few days. A detailed auditory, vestibular, and facial nerve function examination is performed initially and 6 to 8 weeks after trauma to diagnose abnormalities and determine treatment or sequence progress.

Patients with basilar skull fracture who have immediate complete facial nerve paralysis and temporal bone fracture are considered for high-dose steroid treatment or surgical exploration to decompress or graft the nerve. Patients with delayed onset of the facial paralysis or those who initially have only facial paresis are treated with steroids, and observed, because some spontaneous recovery frequently occurs.

Maxillofacial Injuries

Skull and maxillofacial fractures often coexist after head trauma. For instance, fractures of the frontal bone or basilar skull commonly extend into the orbit, and midfacial fractures frequently accompany frontal skull, frontal sinus, or orbital fractures. In addition, fractures through the skull into the nasal sinuses can cause dural lacerations with CSF leak or pneumocephalus. When maxillofacial injury is suspected on physical examination, a CT scan of the face is the most useful diagnostic test and should be obtained at the time of the initial radiographic survey. Facial CT scans should consist of bone and soft tissue windows and axial and coronal sections.

Assessment

The events of the injury should be ascertained and a complete history of the accident or injury should be reached as described by the emergency medical technician, patient, or family members. A thorough facial physical examination is performed in sequence, concentrating on functional deficits in areas of injury. Consultations from specific specialists, such as an ophthalmologist, are also obtained. Cranial nerve abnormalities may also accompany facial fractures; oculomotor deficit, facial sensory deficit, and visual deficit are some common symptoms.

Soft tissue injury implies the possibility of damage to deeper structures, which should be presumed until appropriate examination excludes them. Hematomas are usually diffuse, and not amenable to aspiration, but localized hematomas can be aspirated or removed to facilitate healing. Lacerations should be carefully debrided and repaired after damage to bones and deep soft tissue structures has been determined.

The facial bones should be examined in a methodical sequence from top to bottom. Symptoms that imply bone injury include soft tissue injury (contusion, laceration, hematoma), bone movement, crepitation, localized tenderness, discomfort, numbness in the distribution of a cranial sensory nerve, paralysis in the distribution of a cranial motor nerve, malocclusion, visual acuity disturbance, diplopia, facial deformity or asymmetry, intraoral lacerations, fractured or avulsed teeth, air in soft tissues, and bleeding from the nose or mouth. The examiner should palpate the symmetry of the facial bones, comparing both sides. In all cases reference to old photographs (such as a driver’s license) are valuable aids in documenting a preexisting facial deformity or in establishing a change from previous appearance. Dental malalignment (malocclusion) is an index of bone or tooth fracture, edema, or temporomandibular joint injury.

Facial sensation is noted in the supraorbital, supratrochlear, infratrochlear, infraorbital, and mental nerve regions of the trigeminal nerve distribution for both pinprick and light touch sensation. Diminished sensation in the distribution of a specific sensory nerve indicates injury from transaction, impact, or continued compression of the nerve as the result of a fracture. The facial nerve is tested by comparing facial expression bilaterally. Extraocular movements and pupil response are compared, evaluating symmetry, pupil size, and the speed of pupil reaction bilaterally to both direct and consensual responses to light.

Emergency treatment is immediately directed toward life-threatening events such as (1) airway obstruction, (2) bleeding (major hemorrhage from the scalp or face), and (3) aspiration (prevented when the airway is maintained by orotracheal intubation, although occasionally an emergency cricothyroidotomy is required). The stability of the cervical spine is assessed in every patient with head trauma during this phase.

The early management of maxillofacial injuries is based entirely on a good clinical examination and facial CT scans (Fig. 22.11). Soft tissue windows are necessary on the CT scan to evaluate the brain and orbital soft tissue fully. Axial (Fig. 22.12) and coronal CT bone windows (direct or reformatted) are crucial to reveal details of fractures of the upper face and orbit. Coronal sections (Fig. 22.13) begin with the nasal pyramid and continue posteriorly through the orbital apex. Axial scans begin at the superior aspect of the skull and progress through the brain with standard axial brain imaging. The size and spacing of the cuts at the level of the frontal sinus are reduced to 5 mm or less to obtain the required detail. When a mandible fracture is suspected, the axial CT scanning is continued through the entire mandible and temporomandibular joints, visualizing both the horizontal and vertical portions of the mandible and the temporomandibular joints. Although three-dimensional reconstruction with shading (Fig. 22.14) adds spatial information, it does not provide the detail of two-dimensional axial and coronal images. In some cases, special reconstructions, as one performed in the longitudinal axis of the optic nerve in orbital injury, provide additional information.

FIGURE 22.11 Two-dimensional facial computed tomography (CT) scans are essential in facial fracture evaluation. They can be rapidly obtained after the CT evaluation of the brain. Axial and coronal windows should be obtained through the entire area of the injury. Here, coronal CT scans demonstrate reduction of a zygomatic fracture by plate and screw fixation and orbital floor bone grafting.

FIGURE 22.12 Axial window of an orbital fracture. The globe is prolapsing into the floor defect.

FIGURE 22.13 Direct coronal windows are preferable for evaluation of the orbit, sinuses, and palate. Both soft tissue (A) and bone (B) windows should be obtained for the orbit. Two blow-out fractures are seen. In A the inferior rectus muscle is adjacent to the fracture. In B soft tissue windows clearly show the inferior meatus muscle adjacent to the fracture. C, Reformatted images may be obtained where the direct coronal image is not possible. Their clarity depends on the axial cuts.

FIGURE 22.14 Three-dimensional computed tomography (CT) scans add spatial perspective, but they do not replace two-dimensional CT scans and are not essential for fracture repair. A depressed zygomatic and orbital fracture is seen.

Associated Conditions

Facial Fracture Classification by Anatomical Region

The treatment of maxillofacial fractures is organized by anatomical region (Fig. 22.15). The frontal bone region includes the frontal bone, the supraorbital rims bilaterally, and the frontal sinus (Fig. 22.16). The upper midface region includes the zygoma laterally, the internal orbital area, and the nasoethmoidal area centrally. The lower midface consists of the maxillary alveolus. The mandible consists of the horizontal portion containing the teeth and the vertical portion that includes the angle, ramus, coronoid, and condylar process. The pattern and displacement of the fractures in each anatomical region determine treatment. Orbital fractures are classified by their position on the orbital rim and by their involvement of the internal section of the orbit. Orbital rim fractures are divided into supraorbital, the nasoethmoid medically, and the zygomatic region inferolaterally (Fig. 22.17). The section of the internal orbit consists of the orbital floor, the lateral orbit, and the medial (ethmoidal) orbit. Maxillary fractures are classified according to the patterns of Le Fort, based on the fracture’s location in the maxilla where it is separated from intact upper facial units.

FIGURE 22.15 The anatomical regions of the face are shown. They include the frontal bone, the frontal sinus, the nose, the nasoethmoidal area, the zygoma, the internal orbit, the maxilla, and the mandible.

FIGURE 22.16 The divisions of the frontal bone area are shaded. They include the central (frontal sinus) area (blue) and, laterally, the frontal-temporal-orbital region (green), which extends to the coronal suture. Fractures often involve two of three areas of the frontal skull.

FIGURE 22.17 The orbit consists of three sections from anterior to posterior: (1) the thick rim anteriorly; (2) the thin middle section; and (3) the thick posterior third of the orbit. The posterior portion of the orbit represents the cranial base. The orbital rim can be conceptualized in three regions: superiorly, the supraorbital rim; inferiorly and laterally, the zygomatic region; medially, the nasoethmoidal area.

Fractures of the Frontal Bone and Supraorbital Area

Fractures of the frontal bone area frequently extend to the orbital roof, frontal sinus, and nose. A fracture in this area implies the possibility of injury to the dura and to the frontal lobes. CSF rhinorrhea and pneumocephalus may be present. Because of its strength, the frontal bone is involved in only 5% to 10% of all fractures. Fractures that simultaneously involve the cranium and the orbit are high-energy injuries, and soft tissue damage is more severe. Major injuries to the brain and the cervical spine frequently accompany these fractures, and contusions of the forebrain and orbital contents are routine.

The frontal and ethmoid sinuses render the frontal bone more vulnerable to injury and infection. Each major segment of the frontal sinus (generally two) has a “duct” (usually a broad ostium) that communicates with the middle meatus of the nose. Sinus injury may therefore result in duct obstruction after fracture, mucosal edema, or damage (Fig. 22.18). A cyst-like structure called a mucocele (obstructed mucous cyst) sometimes follows mucosal injury; depending on size, it may create eroding bone pressure and penetrate into the orbit or intracranial cavity. Surgery at a later time is necessary to remedy either of these conditions, as symptoms of pain and sinusitis will persist. Because the posterior wall of the frontal sinus is in contact with the dura, any infection in that area represents an extradural abscess. Posterior wall fractures of the frontal sinus are often accompanied by dural tears. Many of these tears extend along the anterior frontobasilar region of the skull to cause CSF leak or pneumocephalus. A small CSF leak is often masked by epistaxis in the early days after facial injury. When fractures in the posterior wall of the frontal sinus or the anterior base of the skull are noted, a CSF leak should be suspected.

FIGURE 22.18 A fracture and frontal sinus duct obstruction are visible on this plain film. A mucocele might have a similar appearance.

Fractures of the frontal bone commonly extend within the cranial sutures and then involve other regions. When the fracture extends into the supraorbital region, the bone is usually depressed downward and posteriorly, compressing the orbital contents and producing a downward and forward dislocation of the globe (Fig. 22.19). With more limited injuries, linear frontal skull fractures may extend into the orbit and along the cranial base. These fractures can create a CSF leak or obstruct sinus drainage by edema or bone displacement. As fracture patterns become more complex and severe, bone displacement occurs. The anterior base of the skull and the roofs of the orbit are comminuted, and linear fractures extend from the anterior through the middle cranial fossa. The anterior and middle sections of the orbit displace, absorbing energy, and linear fractures extend from the displaced bone through the posterior portion of the orbit and into the middle cranial fossa. These fractures can account for basilar CSF leaks, pituitary disturbances, and dizziness from involvement of the temporal bone and vestibular structures.

FIGURE 22.19 In the supraorbital fracture, posterior and inferior displacement of the superior orbital rim produces downward and forward dislocation of the globe. A, The normal configuration of the superior orbit. B, Dislocation of the superior orbital rim and globe displacement. C, A patient with a displaced supraorbital fracture producing inferior globe displacement.

Diagnosis

The most common clinical signs of fractures of the frontal bone are a bruise or hematoma over an area of blunt injury and, less often, a laceration of the brow or the central forehead. CT scans occasionally show a posterior wall fracture of the frontal sinus without accompanying anterior wall fracture. Fractures of the orbit usually result in palpebral and subconjunctival hematomas. A step deformity or irregularity in the orbital rim may be appreciated on palpation, but swelling may obscure the irregularity. If periorbital swelling is severe, complete ptosis exists. If the lid cannot be opened voluntarily, it should be opened manually to inspect the globe for integrity. Visual acuity should be assessed and extraocular muscle motion should be evaluated where possible.

Evaluation of the visual system is critical. Supraorbital fractures, for example, represent 10% of all periorbital fractures but account for 30% of serious eye injuries. The most common serious injuries to the globe are rupture, retinal detachment, and vitreous or anterior chamber hemorrhage. The presence of globe injury modifies fracture treatment by severely limiting manipulation; avoidance of any pressure on the globe may take precedence over bone reconstruction. Visual acuity and pupil response are documented before and after any surgical treatment using a Rosenbaum pocket visual screening card. If this is not possible, the pupillary response to light is evaluated both directly and consensually. Inability to move the globe into a particular field of gaze indicates either a cranial nerve palsy or interference with an extraocular muscle secondary to contusion, local nerve injury, or incarceration of an extraocular muscle or its adjacent soft tissues.

Fractures of the roof of the orbit usually produce a temporary paresis of the levator muscle that results in post-traumatic ptosis. This palsy may persist for months; no treatment to elevate the lid further is indicated until all chance of spontaneous recovery has been permitted (at least 6 months). Partial or complete spontaneous recovery usually occurs. The superior rectus muscle is usually undamaged in fractures of the superior orbit, but occasionally paresis occurs and mimics incarceration of the inferior rectus muscle (failure to elevate the globe). These conditions are differentiated by the combination of radiographic evaluation, forced-duction testing, and formal eye muscle evaluation. Entrapment of the levator or superior rectus muscles rarely occurs in orbital roof fractures.

Supraorbital fractures involving the orbital rim are usually displaced inward and downward (see Fig. 22.19), producing a forward and downward displacement of the globe. The globe occasionally bulges forward so that the eyelids cannot close completely. In such cases urgent facial fracture reduction is required to protect the cornea. Fractures of the orbital roof may have a linear extension that enters the superior orbital fissure or optic foramen. Visual acuity is affected if the optic nerve is compressed by a displaced fracture fragment or by edema or nerve shearing, in which case direct pupillary response to light on the injured side is slower than the direct pupil response on the other side. A superior orbital fissure syndrome may also be present, consisting of variable palsy of extraocular muscle motion (cranial nerves III, IV, VI), ptosis, global proptosis, and anesthesia in the first division of the trigeminal nerve (the ipsilateral forehead) (Fig. 22.20 and see section on Orbital Fractures). Patients may experience numbness in the distribution of the supraorbital and supratrochlear nerves, which is usually transient, although lacerations in the area frequently divide the nerve, producing permanent numbness.

FIGURE 22.20 The contents of the superior orbital fissure include cranial nerves III, IV, and VI, the ophthalmic division of (trigeminal) cranial nerve V, and vascular structures. The optic foramen is contained within the lesser wings of the sphenoid and admits the optic nerve and ophthalmic artery.

Management

Displacement of the roof and rim of more than 4 or 5 mm produces a depression and a forward movement in globe position; release of the pressure on the globe or the nerves may improve function. Open skull fractures require débridement, repair of dural lacerations, evacuation of epidural hematomas, and appropriate surgical procedures for frontal lobe injury. Bone fragments are cleaned of mucosa and debris, and antiseptic irrigation is used. The frontal skull can be reconstructed primarily by linking the bone fragments with wires or plate and screw fixation, stabilizing the pieces securely.

Frontal Sinus Fractures

Fractures of the frontal sinus may involve the anterior wall, the posterior wall, or both. Fractures that obstruct the nasofrontal duct must be treated by eliminating the function of the sinus. Fractures that depress only the anterior wall of the frontal sinus are repaired for esthetic reasons. The symptoms of a frontal sinus fracture include localized bruising, hematoma, or lacerations; the fracture often extends into the orbit, producing both palpebral and subconjunctival hematomas (spectacle hematoma).

Diagnosis

Frontal sinus fractures are diagnosed on CT scan noting fractures of the front wall, back wall, duct, or both walls. Displacement of bone of the posterior wall more than the thickness of the bone wall usually indicates an underlying dural laceration.

Management

Localized fractures of the anterior wall are managed by returning the bone fragments to the proper position and debriding any devitalized mucosa. If the nasofrontal duct is intact, fluid will flow freely into the nose; replaced bone fragments are stabilized with plate and screw fixation. If the posterior wall is involved, the integrity of the dura is usually assessed by direct inspection at operation. Significant fractures of the anterior and posterior walls are best managed by intracranial exposure and débridement of small bone fragments, and defunction of the sinus. If the posterior wall of the sinus is removed, the sinus is “cranialized” by completely removing the mucosa and plugging the nasofrontal duct with several layers of bone grafts. A sheet bone graft is placed over the bone plugs and over the involved ethmoid sinuses (Fig. 22.21). Involved sinus must be debrided to minimize infection and delayed mucocele formation because obstruction of an ethmoid sinus produces an orbital or epidural abscess. The anterior wall of the frontal sinus is then reconstructed. Complete removal of sinus mucosa requires mucosal stripping and light burring of its bone fragments as the mucosa has minute invaginations (foramina of Breschet) into the bone.

FIGURE 22.21 The nasofrontal duct should be plugged with several layers of bone graft. Bone provides strong structural material to close the opening between the intracranial cavity and the nose. Muscle and fascia deteriorate rapidly and do not provide stability.

Less complicated frontal sinus fractures may be managed by another more limited procedure which defunctionalizes the sinus “obliteration.” When fractures compromise nasofrontal duct function, the sinus mucosa should be removed and the walls of the sinus should be burred to bleeding bone. The nasofrontal duct is then plugged with several layers of bone plugs taken from the calvaria, and the remainder of the sinus is filled with bone shavings (Fig. 22.22). Unfortunately, regrowth of frontal sinus mucosa may occasionally occur, or the development of a cyst in a lacerated area of mucosa may produce a mucocele. Surgical intervention may be required for infection or erosion of the cyst into adjacent structures.

FIGURE 22.22 A, A sheet bone graft should be laid across the plugged frontal sinus ducts to cover previously cleansed and débrided fractures involving the cranial base and ethmoidal sinuses. This layer is not watertight but begins to develop its own partition between the intracranial cavity and the nose. B, In cases in which the sinus cavity is to be obliterated, the mucosa is thoroughly removed. The walls of the sinus should be burred lightly to eliminate areas where mucosa extends along the veins into the bony walls of the sinus cavity. After nasofrontal duct obliteration with bone plugs, the sinus cavity can be obliterated with particulate bone graft (C) taken from the parietal area with a craniotome (D).

Orbital Fractures

The supraorbital rims are weakened centrally by the presence of the frontal sinus. The supraorbital rim extends to join the temporal bone and the zygoma (see Fig. 22.17). The orbit cavity itself has three sections (see Fig. 22.17): the anterior or rim, the middle, and the posterior orbit. The midsection of the orbit can be divided into four regions (see Fig. 22.17) and the rim into three sections. Fractures occur first in the thin bone of the middle third of the orbit, then the rim. This sequence protects the posterior orbit fractures from much displacement.

A blow to the lateral aspect of the upper face can fracture both the supraorbital rim and the zygoma. Cranio-orbital injuries call for both neurosurgery and orbital reconstruction. Zygomatic fractures usually extend from the junction medially with the maxilla at the infraorbital rim through the inferior and lateral orbit. Medially, the fracture often involves the canal for the infraorbital nerve, which is located 8 to 10 mm inferior to the lower orbital rim, parallel to the medial aspect of the cornea. A fracture here produces numbness in the infraorbital nerve distribution.

The nasoethmoidal orbital region represents the medial rim and medial wall of the orbit (Fig. 22.23). Posteriorly, the ethmoid air cells weaken the nasoethmoidal region, one of the thinnest portions of the orbital wall. Fractures involving the medial orbital rim displace the bone bearing the attachment of the medial canthal tendon posteriorly and laterally, which may also block the lacrimal system, resulting in tearing. Displacement of the medial orbital rim or the infraorbital rim and floor of the orbit alters the medial attachment of the eyelids and the suspensory ligaments of the globe, permitting globe and canthal ligament dystopia and telecanthus, which can be detected on physical examination.

FIGURE 22.23 A, The medial wall is the thinnest bone of the orbit but, reinforced by septa within the ethmoid sinus, it is stronger than its thickness implies. The anterior and posterior ethmoidal foramina, located toward the upper portion of the medial orbital wall, are on the same level as the optic canal. These neurovascular foramina can be used as landmarks to direct the surgeon, warning to protect the optic nerve canal, which is 5 mm from the posterior ethmoid foramen. B, Fractures of the ethmoid frequently show symmetrical compression. Reconstruction involves bone grafting to the normal contour.

The orbital roof is composed of the greater and lesser wings of the sphenoid. It separates the anterior cranial fossa from the orbital contents. Medially, at the frontal sinus, the orbital roof thins, becoming almost transparent. The attachment of the superior oblique tendon immediately behind the rim is often a separate small fragment in fractures. Diplopia produced by interference with superior oblique function is difficult to remedy. The surgeon must be aware of this attachment and carefully avoid injury by making dissection exactly subperiosteal beyond the confines of the muscle. The frontal sinus is extremely variable in size and shape, and asymmetry is the rule. It does not develop until the teenage years and thus is absent in the pediatric trauma victim.

The medial wall of the orbit is formed by the thin orbital plate of the ethmoid bone. This bone is reinforced by septa within the ethmoid sinus, which gives it some additional strength (see Fig. 22.23). The lateral wall of the orbit consists of the orbital process of the malar bone anteriorly and the greater wing of the sphenoid posteriorly (Fig. 22.24). The zygomaticosphenoid suture is involved in all zygoma fractures with the exception of those confined to the zygomatic arch. Its broad surface forms an excellent area for confirmation of proper zygomatic alignment at the time of reduction. With more comminuted orbital fractures, displacement of multiple walls of the orbit contributes to dramatic orbital deformity. Because soft tissue orbital deformity is not entirely reversible with secondary corrections, the emphasis is on immediate anatomical reconstruction.

FIGURE 22.24 The lateral wall of the orbit. Often, the anterior portion of the greater wing of the sphenoid fractures and is involved in expansion of the orbital cavity. The distances of the various structures from the rim are shown.

The lateral canthal ligament is attached with the lateral aspect of the eyelids to the zygoma at Whitnall’s tubercle, which is a shallow bulge behind the internal aspect of the lateral orbital rim about 10 mm inferior to the zygomaticofrontal suture. The anterior limb of the lateral canthal tendon is continuous with the galea, and the posterior limb joins the lateral extension of the levator tendon and Lockwood’s suspensory ligament in its attachment to Whitnall’s tubercle (Fig. 22.25). The extraocular muscles travel close to the orbital walls in the posterior half of the orbit, In the anterior half of the orbit, they are protected from orbital wall fractures only by a thin cushion of extramuscular cone fat. Thin “muscular cheek ligaments” extend from the extraocular muscles diffusely to the orbital walls (Fig. 22.26). The fine ligament system, described by Leo Koorneef (see Fig. 22.26), diffusely interconnects the soft tissue of the orbit to provide structural continuity among all the orbital tissues, such as fat, muscle, periosteum, and globe. This interconnection of all orbital soft tissue is why diplopia (extraocular muscle restriction) occurs if a particular section of orbital fat is trapped in a fracture by virtue of these connections. The entrapped fat and ligament system, in the absence of actual extraocular muscle incarceration, may cause diplopia.

FIGURE 22.25 The fascial sling for globe support. The globe has been removed. Medially and laterally, the medial and lateral canthal ligaments provide attachments for structures that provide anterior globe support. Indicated are Lockwood’s ligament, supporting the globe inferiorly, the medial and lateral canthal ligaments, and behind them, medial and lateral cheek ligaments. Superiorly, Whitnall’s ligament is present. The combined muscle sheaths also attach to the globe and provide a relative sling for fat and globe support. These ligaments and their sheaths join to Tenon’s capsule.

FIGURE 22.26 Entrapment of the fine ligament system described by Leo Koorneef may produce limitation of extraocular motion. A, The normal system of ligaments that diffusely connect the bony walls of the orbit to the extraocular muscles and the globe. B, An orbital floor fracture has trapped fat and its interconnecting ligaments in the fracture site. Ocular motility may be impaired by impingement of the fine ligament system.

(After Koorneef L. Current concepts in the management of blow-out fractures. Ann Plast Surg 1982:9:185-199.)

The orbital floor is one of the weakest portions of the orbit. There is an initial concave section of the floor immediately behind the inferior orbital rim, and then a convex constriction of the orbit posteriorly. This complex orbital shape must be re-created when reconstructing the orbit. Because the complex curves of bone in relation to the soft tissue determine globe position (Fig. 22.27), it is extremely important to mimic the exact curvature of the middle portion of the orbit and the position of the orbital rim in reconstruction. The concave orbital roof must be reconstructed in its exact arching anatomical position, or the globe will be displaced inferolaterally. The orbital roof is convex from anterior to posterior, and from medial to lateral.

FIGURE 22.27 The curves of the orbit in the longitudinal axis of the optic nerve. The normal configuration (top) and the usual configuration in enophthalmos (bottom) of the orbital floor are indicated. An intact ledge of bone is present in the posterior orbit and provides a guide for the floor reconstruction. First, the orbital rim should be properly positioned. The intact posterior ledge of bone provides a scaffold for bone support between the rim and the posterior orbit. The soft tissue prolapsing into the maxillary sinus must be elevated, restoring globe position.

The posterior third of the orbit contains the optic foramen, the superior orbital fissure, and the posterior aspect of the inferior orbital fissure. The superior orbital fissure is bounded by the greater and lesser wings of the sphenoid (see Fig. 22.20). Linear fractures are commonly seen in the posterior portion of the orbit; however, displacement of bone is less common. Usually, the anterior and middle sections of the orbital bones displace, acting as a “shock absorber” protecting posterior orbital bone from severe displacement.

The inferior orbital fissure separates the orbital floor from the lateral orbital wall. It contains veins, the infraorbital artery and nerve, and the zygomaticofacial nerve.

Diagnosis

A mobile or absent orbital roof may allow pulsating exophthalmos, in which cerebral pulsations are transmitted to the globe and its adnexal structures. This is corrected by reconstruction of the roof, separating the orbit from the intracranial contents with a bone graft.

Fractures involving the orbital roof and middle cranial fossa may sometimes create a communication (carotid-cavernous sinus fistula) between the carotid artery and the cavernous sinus. A traumatic carotid-cavernous fistula is usually accompanied by severe visual and cranial nerve disturbances. Marked chemosis, globe prominence, extraocular muscle palsy, and blindness are usually present. The fistula is confirmed by arteriography; attempts to obliterate it involve intravascular radiographic embolization techniques.

The most common reason for visual acuity deficit after trauma is optic nerve injury. Shearing, contusion, or compression may be involved. These injuries may occur with or without demonstrated fractures of the optic canal. If vision is lost at the moment of impact, decompression of an optic canal fracture usually does not increase the chance of visual recovery. Frequently, steroids are employed but recently their efficacy has been questioned. When bone displacement that compromises the optic canal is demonstrated, or if fluctuating or deteriorating visual deficit is seen, then optic canal decompression should be considered. Immediately after an optic nerve injury, the optic disk usually looks normal. A patient with visual loss may present with a Marcus Gunn pupil, in which the reaction to consensual constriction is present but the reaction to direct stimulus is reduced. Swinging a light from one eye to the other demonstrates paradoxical pupillary dilatation in the affected eye (Fig. 22.28).

FIGURE 22.28 The normal pupil reflex pathway and the relation for the Marcus Gunn pupil. In the normal eye, light striking the retina produces an impulse in the optic nerve that travels to the pretectal nucleus, both Edinger-Westphal nuclei, via nerve III to the ciliary ganglion and papillary constrictor muscles. In lesions involving the retina or optic nerve back to the chiasm, a light in the unaffected eye produces consensual constriction of the pupil of the affected eye, but a light in the affected eye produces a paradoxic dilatation of the affected pupil.

(After Jabaley ME, Lerman M, Saunders HJ. Ocular injuries and orbital fractures: a review of 199 cases. Plast Reconstr Surg 1975:56:410.)

Atrophy of the optic disk does not appear until 1 month after an optic nerve is injured, so it cannot be used as an acute indication of optic nerve damage. If vision is initially present after an injury and then deteriorates, swelling from hemorrhage and edema may be compromising the optic canal, compressing the optic nerve. Surgical decompression or medical (high-dose steroids) decompression are indicated on an emergency basis for such delayed nerve function loss. Some feel that optic nerve injury with no light perception should be treated routinely with canal decompression, but the prognosis for this injury remains poor no matter what is done.

Nasoethmoid Orbital Fractures

The nasoethmoid orbital fracture consists (in its simplest form) of injury to one or both frontal processes of the maxilla (medial orbital rims) with their attached canthal ligaments and the nose. The frontal process of the maxilla is the lower two thirds of the medial orbital rim. When this is fractured, the medial canthal ligament is displaced because of its attachment to the fractured bone segment. Nasoethmoid fractures often extend to adjacent areas, including the supraorbital region, the frontal sinus, the zygoma and inferior orbital rim, the medial internal orbit, and the orbital floor.

These injuries, which may cause significant long-term deformity of telecanthus and enophthalmos, are often initially obscured by swelling. Patients usually present with bleeding from the nose, a nasal dislocation, and bilateral periorbital and subconjunctival hematomas (Fig. 22.29). The nasal deformity consists of depression of the nasal dorsum and foreshortening of the nose, with an increased angle between the columella and the lip. Severe dislocation of the septum and nasal septal perforation are often present. Forty percent of nasoethmoid fractures are unilateral, and because of their proximity to the frontal sinus and the dura, a CSF leak may be present. Nasoethmoid fractures produce tearing by compromising the drainage of the lacrimal system as it passes through the maxilla. On palpation, pain and tenderness are found over the frontal process of the maxilla, and the palpating finger, inserted deeply over the medial canthal ligament, discloses bony crepitus, movement, and tenderness. Telecanthus may be present if the medial orbital rim fracture fragment has been dislocated laterally, in which case the palpebral fissure shortens.

FIGURE 22.29 A, In most patients with nasoethmoidal fractures, severe midfacial injury is obvious. Bilateral periorbital hematomas are routine. Here, the nose has literally been driven into the midface and is depressed along its dorsum with foreshortening of the length (increased angle between the lip and columella). B and C, Computed tomography scans of the nasoethmoidal orbital fracture demonstrate comminution of the entire medical orbit and nose.

Diagnosis

The presence of a nasoethmoid fracture can be determined by a bimanual examination (Fig. 22.30). A palpating finger is placed deeply over the canthal ligament opposite a clamp placed intranasally, and the “central” (canthal ligament containing) bone fragment is moved between the finger and clamp. Movement confirms a mobile base fracture.

FIGURE 22.30 The bimanual examination is performed by placing a clamp inside the nose with its tip immediately adjacent to the attachment of the canthal ligament on the frontal process of the maxilla. It is important that the clamp not be placed beneath nasal bones or a false positive diagnosis of a nasoethmoidal fracture will be obtained. A palpating finger is placed externally deeply over the canthal ligament. If the frontal process of the maxilla can be moved between the clamp and the palpating finger, a nasoethmoidal fracture is present. Mobility requires surgical reduction.

On CT scan, fractures surround the lower two thirds of the medial orbital rim, medial and inferior internal orbital fractures are present, and the inferior orbital rim, piriform aperture, nose, and internal angular process of the frontal bone at the glabella are fractured.

Lacrimal system injury should be suspected in lacerations of the medial portion of the eyelids. The lacrimal system may also be compromised by fractures involving the bone surrounding the nasolacrimal duct. If the lacrimal system is transected, fluid emerges from a laceration on irrigation of the system with saline by a catheter placed through the lacrimal punctum in the lower lid.

Management

Nasoethmoid orbital fractures require a definitive open reduction consisting of interfragment wiring and plate and screw fixation of the assembled fragments. In some situations, this can be accomplished through a laceration or local incision; otherwise, a broad exposure must be provided by a coronal incision (Fig. 22.31), bilateral lower eyelid incision, and gingival buccal sulcus incision. Usually, the surgeon is careful to avoid detaching the canthal ligament from the bone during fracture reduction. If the canthal ligament is detached by the injury, it must be reattached after assembly of the bone fragments to the proper area of the medial orbital rim. A separate set of transnasal wires, again passed posterior and superior to the lacrimal fossa through the nose, connect the canthal ligament to the bone in its proper position (Fig. 22.32) after the bone reduction. Contoured bone grafts are used to reconstruct the medial and inferior internal orbit (Fig. 22.33). Long straight bone grafts are used to provide contour and to add dorsal height to the nose. These bone grafts are taken from the calvarium, the iliac crest, or a split rib.

FIGURE 22.31 Exposure of the entire medial (nasoethmoidal orbital) section is provided by a coronal incision with dissection of the supraorbital area, orbital roofs, and lateral orbit.

FIGURE 22.32 A, Treatment of a simple nasoethmoidal orbital fracture by plate and screw fixation. Noncomminuted fractures can be treated in this fashion. B, Comminuted fractures require a thorough connection of all fragments with interfragment wires. The essential step in the treatment of a nasoethmoidal orbital fracture is to pass a wire between both medial orbital rim segments. This wire is passed transnasally posterior and superior to the lacrimal fossa.

FIGURE 22.33 The usual internal orbital fractures involving the orbital floor (A) and the medial orbital wall (B). Bone grafts can be used to restore internal orbital integrity.

If a fracture compromises the lacrimal system, replacement of bone into its normal position is the initial treatment. If the lacrimal system is transected, a direct repair of lacrimal canalicular transaction is performed with fine sutures under magnification over fine tubes (0.025 in; 0.6 mm). Both the upper and lower puncta should be intubated and the tubes should be brought into the nose through the nasolacrimal canal. They should remain in place for several months to splint the lacrimal system repair.

Fractures of the Orbital Floor

The bony orbital space is a modified cone or pyramid. Fractures of the inferior portion of the orbital floor often extend 30 to 35 mm behind the rim. The presence of the intraorbital nerve canal weakens the orbital floor. Fractures of the rim and floor usually impair the function of the nerve, producing hyperesthesia of the upper lip, ipsilateral nose, and anterior maxillary teeth.

The most frequent fracture of the internal orbit is the blow-out fracture, which is usually confined to the floor and the lower portion of the medial wall (Fig. 22.34). A depressed fracture of this section of the orbit allows the orbital tissue to be displaced downward into the maxillary and ethmoid sinuses. Medial, inferior, and posterior dislocation of the globe occurs. If fat is trapped in the fracture, it may interfere with the motion of the globe because of the fine internal ligament system of the orbit linking all soft tissue (see Figs. 22.34 and 22.26). Less commonly, the inferior rectus muscle may be directly trapped in a small fracture, leading to restriction of globe movement. Patients with orbital fractures usually present with a history of a blunt injury to the orbit. They may have double vision when looking either upward or downward. Extraocular range of motion may be limited. Periorbital and subconjunctival hematomas are present and there may be numbness in the infraorbital nerve distribution. It is imperative that the globe be examined; the possibility of hyphema, retinal detachment, or globe rupture exists with any fracture involving the orbit.

FIGURE 22.34 A and B, An orbital blow-out fracture involving the thin portion of the orbital floor. Fat and its interconnecting fascia are trapped among the blow-out fragments and limit the excursion of the inferior oblique and inferior rectus muscles. Diplopia may be present from muscle restriction in either up- or downgaze.

The possible presence of an intraorbital foreign body should also be considered. Orbital fractures are accompanied in 10% to 15% of cases by a globe injury. The visual system and globe are evaluated by visual acuity, visual fields, funduscopic examination, extraocular motion, and intraocular pressure.

Diagnosis

When an orbital floor fracture is accompanied by diplopia, the “forced-duction” test is used to confirm incarceration of orbital soft tissues in the fracture site. Absence of rotation on attempted globe rotation documents muscle or extraocular system tissue restriction. A “force-generation” test provides additional information by demonstrating “pull” generated by extraocular muscles when the globe is held by forceps and globe rotation is attempted by the patient. Globe entrapment by tethering soft tissue occurs most frequently with small orbital fractures. Enlargement of the orbital volume is generally produced by large fractures; globe dystopia and enophthalmos are the result of significant orbital cavity enlargement.

Enophthalmos denotes the backward dislocation of the globe into the orbit (Fig. 22.35). Large fractures of the orbital floor allow the orbital soft tissue to prolapse backward, downward, and medially, resulting in a loss of globe support and a change in globe position. The position of the globe on physical examination is best compared by assessing symmetry in the patient with an inferior view (Fig. 22.36) or with Hertel exophthalmometry. The trauma of the injury may produce periorbital fat atrophy, which may cause globe malposition. Acutely, periorbital injuries produce hemorrhage and edema. Initially, proptosis or exophthalmos appears. Acute enophthalmos is unusual and indicates a dramatic enlargement in the orbit. If the globe prolapses away from the lids, lubrication of the cornea cannot be accomplished; this is an urgent indication for orbital wall repair. Enophthalmos is usually accompanied by inferior displacement (globe dystopia). Posterior displacement of the globe produces a supratarsal hollow and ptosis of the upper eyelid.

FIGURE 22.35 The orbit’s enlargement allows displacement of the globe backward and downward to produce enophthalmos.

FIGURE 22.36 Enophthalmos is most accurately assessed by comparison of globe position from an inferior perspective.

Management

In many cases, the symptoms of a small internal orbital fracture resolve substantially within a short period. Frequently, double vision is the result of muscular contusion and resolves with observation. Surgery is usually indicated for double vision only when it occurs in a functional field of gaze and is the result of incarceration of the muscle or the ligament system. There are thus two indications for surgery for blow-out fractures: muscle or ligament entrapment confirmed by CT scan and forced-duction examination, and enlargement of the orbit sufficient to produce enophthalmos. This generally requires more than 2 cm² of orbital floor involvement, with displacement of that section more than 3 to 4 mm. The size of the fracture can be accurately estimated on CT scans. The orbit should be reconstructed by bone grafts or alloplastic material placed over the edges of the orbital defect so as to support the orbital contents (see Fig. 22.33).

Le Fort Maxillary Fractures

Fractures of the maxilla involve not only the lower maxilla but often the entire midfacial region. These fractures are termed Le Fort maxillary fractures after the classification used by René Le Fort (Fig. 22.37), who described the three “great lines of weakness” of the maxilla through which fractures commonly occur.

FIGURE 22.37 Le Fort fractures. Le Fort, on the basis of cadaver experiments, identified thinner areas of the midfacial skeleton that fracture more commonly. Often, combinations of fractures are seen. The Le Fort I fracture travels horizontally across the base of the piriform aperture, separating the lower portion of the maxillary sinuses from the upper midfacial skeleton. On the Le Fort II injury, a pyramidal lower facial segment is separated from the upper cranial facial skeleton. The fracture travels laterally at the Le Fort I level, then travels upward through the inferior orbital rims medially, and through either the cartilaginous portion of the nose or the nasofrontal junction centrally. In the Le Fort III injury, the cranium is separated from the midfacial skeleton through the internal orbital margins of the zygoma. The fracture begins at the zygomaticofrontal suture, extends down the junction of the greater wing of the sphenoid with the orbital process of the zygoma, crosses the orbital floor to travel up the medial orbital wall, comminutes the nasoethmoid region and the nasofrontal junction, and similarly transects the contralateral orbit. In practice, it is usual to see the Le Fort fracture level higher on one side than the other. Commonly, Le Fort III superior level injuries occur on one side with a Le Fort II superior level injury on the other side.

Diagnosis

In 10% of the Le Fort fractures the maxillary alveolus itself is split, usually in a sagittal (longitudinal) direction (Fig. 22.38), increasing instability and making preservation of normal occlusion a challenge. Lower maxillary fractures are diagnosed by malocclusion and maxillary mobility. Upper maxillary fractures are diagnosed by maxillary mobility, malocclusion, periorbital hematomas, nasopharyngeal bleeding, pain, and the symptoms of zygomatic, orbital, and nasoethmoidal fractures. Examination for maxillary mobility is essential to confirm the presence of a Le Fort fracture. The level at which the mobility occurs indicates the level of the Le Fort fracture. The maxilla should be grasped with one hand while the head is stabilized with the other. The level at which the mobility occurs indicates the level of the Le Fort fracture. Multiple Le Fort fracture levels may be seen in the same patient. Occasionally, Le Fort fractures are not mobile; they may be either impacted or incomplete.

FIGURE 22.38 A, Sagittal fracture of the maxilla. B, Open reduction and internal fixation using small plates and screws is being performed in the roof of the mouth for this sagittal fracture of the palate.

Management

The principal treatment of Le Fort fractures is intermaxillary fixation with the maxilla in occlusion with the mandible. Initial stabilization is generally accomplished by ligating the arch bars to the upper and lower teeth and connecting the maxillary and mandibular arch bars with intermaxillary wires. Fracture sites at the various levels of the midface (as defined by CT scans) are aligned, and then the nasofrontal and zygomaticomaxillary buttresses (Fig. 22.39) are reconstructed with direct plate and screw fixation. This eliminates or decreases the need for intermaxillary fixation postoperatively.

FIGURE 22.39 A, Treatment of a Le Fort fracture begins with intermaxillary fixation. B, The internal buttress system of the maxilla must be restored by assembling the fragments and stabilizing them with interfragment plate and screw fixation. Here anterior, middle, and posterior maxillary buttresses are seen. The anterior and posterior buttresses are stabilized with rigid fixation, and the posterior buttress by intermaxillary fixation to an intact mandible.

A Le Fort I fracture is treated by placing the patient in intermaxillary fixation, exposing the four Le Fort I level buttresses, reducing the fracture, and using direct plate and screw fixation over the buttress fractures (Fig. 22.40). Bone grafts should span bone gaps of more than 3 to 5 mm.

FIGURE 22.40 Diagram of Le Fort I fracture treatment.

Le Fort II fractures are treated by placing the patient in intermaxillary fixation. The fracture fragments are aligned and stabilized with direct plate and screw fixation (Fig. 22.41). Orbital floor defects are spanned with bone grafts, or perhaps with alloplastic implants for smaller defects. If rigid fixation is used, intermaxillary fixation may frequently be discontinued early postoperatively. Normal occlusion must be confirmed carefully for a 4- to 12-week period postoperatively. Patients with intermaxillary fixation require a liquid diet and should be placed on a soft diet when it is discontinued. The upper nose may need direct fixation through a coronal incision, and the lower orbital rims are reduced and stabilized through bilateral lower eyelid incisions.

FIGURE 22.41 Diagram of Le Fort II fracture treatment.

Le Fort III fractures are treated with surgical approaches to zygomatic, nasoethmoidal, and orbital floor fractures and these fractures are connected to the maxilla at the Le Fort I level (Fig. 22.42). Again, fragments are initially aligned with interfragment wires and stabilized with plate and screw fixation. A sagittal fracture of the maxilla is directly reduced through the palatal laceration or incision with plate and screw fixation (see Fig. 22.38). A small plate is also placed at the piriform aperture to unite the two maxillary alveolar segments. In some cases, an acrylic splint is placed in the palatal vault to reduce the occlusal relationships. A “panfacial fracture” (Le Fort fractures, plus fractures of the nasoethmoidal and mandibular areas) is shown repaired with plate and screw fixation (Fig. 22.42B). The mandibular subcondylar and symphysis fractures were stabilized prior to the fixation of the Le Fort fracture.

FIGURE 22.42 A, Diagram of Le Fort III fracture treatment using plate and screw fixation. B, Diagram of treatment of panfacial (Le Fort plus mandible) fractures.

Fractures of the Nose

A fracture of the nose may involve the cartilaginous nasal septum, the bony septum, the bony nasal pyramid, or the upper or lower lateral cartilages.

Diagnosis

Two types of dislocations occur in the nasal fractures (see Fig. 22.33): (1) posterior dislocation (shortening or flattening of the nose, resulting in a wider nasal bridge); and (2) lateral dislocation (deviated nose). Any patient with a nasal fracture should have the nasal airway inspected. If a significant hematoma exists along the septum, it should be drained to prevent cartilage necrosis. Patients with nasal fractures usually have swelling over the external surface of the nose. A small laceration is often the clue to the presence of a fracture. Pain, crepitation, and periorbital ecchymoses are present but not confirmed sharply to the insertion of the orbital septum as in periorbital fracture. The most reliable sign of a nasal fracture is epistaxis. Radiographic evaluation of the nose is best performed with a CT scan, which can confirm the nasal fracture and also rule out the possibility of adjacent fractures.

Management

The treatment of nasal fractures generally involves a closed reduction under local or general anesthesia. The septum is replaced into its proper position with Asch forceps. The nasal bones are first outfractured by levering the nasal bone outward to complete the fracture (releasing incomplete components of the fracture) and then digitally remolding the nasal bones into their proper positions. A Doyle nasal splint (containing an airway) supports the reduction of the nasal septum and minimizes bleeding. An external metal or plaster splint is placed over the nasal pyramid for 1 week to protect the nose during the healing period. Nasal fractures frequently display residual mild deformity after this initial “closed” management. If the airway remains compromised by a deviated septum, a formal septal resection to improve respiratory symptoms may be performed after 3 to 6 months. Residual deformity of the nasal pyramid requires late osteotomy of the nose (formal rhinoplasty).

Fractures of the Zygoma

The zygoma forms the lateral and inferior portion of the orbit and supports the lateral areas of the upper midface (Fig. 22.43). The prominent position of the zygoma makes it a frequent recipient of traumatic dislocation. A fracture usually involves the entire zygoma, but may less commonly involve the zygomatic arch alone, which produces a minimal depression in the lateral cheek. Depression of the zygomatic arch may interfere with movement of the coronoid process of the mandible, a symptom requiring reduction. Because complete zygomatic fractures involve the lateral and inferior internal walls of the orbit, they may produce ocular symptoms that require treatment.

FIGURE 22.43 Fracture-dislocation of the zygoma. A, The zygoma attaches to the frontal bone superiorly to the temporal bone through the zygomatic arch, to the maxilla medially and inferiorly, and to the greater wing of the sphenoid through the lateral orbit. All of these surfaces must be aligned in fracture reduction. B and C, A typical fracture dislocation of the zygoma is seen in these computed tomography scans.

Diagnosis

The symptoms of zygomatic fractures are shown in Figure 22.44. The lateral canthus, which attaches to the frontal process of the zygoma, may be dislocated inferiorly, producing an antimongoloid slant to the palpebral fissure. Either swelling or dislocation of the zygoma may interfere with motion of the coronoid process by producing a mild temporary interference with occlusion. Hematomas are observed in the cheek, periorbital area, and upper gingival buccal sulcus. Orbit symptoms produced by the fractures include diplopia, ocular dystopia, and lower eyelid dislocation. Palpation of the orbital rim may demonstrate a “step” deformity or depression. Palpation of the malar eminence, when compared with the normal side, demonstrates retrusion. With a medially dislocated zygomatic fracture, the orbital volume may be constricted, resulting in exophthalmos. With laterally or inferiorly dislocated zygomatic fractures, the orbital volume increases, and enophthalmos occurs.

FIGURE 22.44 A and B, The symptoms of zygomatic fractures almost always include the combination of periorbital and subconjunctival hematomas. Posterior displacement of the malar eminence, a palpable step deformity in the orbital rim, and numbness in the distribution of the infraorbital nerve are frequently present. Bleeding from the ipsilateral nose occurs if the fracture extends into the ipsilateral maxillary sinus. The congested swollen conjunctiva in B is a warning of retrobulbar hematoma and possible globe injury.

Zygomatic fractures should be evaluated with axial and coronal CT scans (including both soft tissue and bone windows) for evaluation of the orbital soft tissue and its relation to the fracture.

Management

Treatment of fractures of the zygoma involves reduction, accomplished through lower eyelid and gingival buccal sulcus incisions, and immobilization with interfragment wires stabilized with plate and screw fixation. Thin bone grafts may be required to replace damaged sections of the zygomaticomaxillary buttress, inferior rim, or walls of the orbit. If the zygomatic arch is laterally dislocated, a coronal incision aids reduction. The coronal incision or an upper lid incision exposes the frontal process of the zygoma.

Initially, dislocated fragments of the zygoma are repositioned and aligned by drilling holes adjacent to the fractures and linking the fragments with small interfragment wires. The fracture fragments are held in position while rigid internal fixation is performed using small plates and screws (Fig. 22.45). If the lateral canthus is detached in the reduction, it should be replaced after bone assembly.

FIGURE 22.45 A, Diagram of an open reduction and internal fixation of the zygoma. B, A strong midface plate is placed at the zygomaticofrontal suture and a thinner microsystem plate at the inferior orbital rim (C). Depending on the comminution of the fracture, the surgeon may need to plate the zygomaticomaxillary buttress or the zygomatic arch (D).

For a medially dislocated fracture of the zygomatic arch, whether isolated or occurring simultaneously with other fractures of the zygoma, a small incision can be made in the temporal hair and the “Gilles” approach used to elevate the zygomatic arch into its proper position. An elevator is placed beneath the temporalis muscle fascia directly on the temporalis muscle, which easily slides under the arch, and the zygomatic arch is levered into its proper position.

Fractures of the Mandible

Mandibular fractures are common facial injuries because the mandible’s prominent position renders it susceptible to trauma. Frequently, multiple fractures are present in the same mandible. Mandibular fractures may be classified as “closed” or “open” and by anatomical location. Mandibular areas such as the subcondylar region, the region of the angle, or the cuspid region (the latter two being weakened structurally by the molar and cuspid teeth, respectively) are well-known anatomical areas. The edentulous mandible most commonly fractures in the body and angle region followed by the subcondylar area.

Diagnosis

The diagnosis of the mandibular fracture is suggested by malocclusion, pain, swelling, tenderness, crepitus, fractured teeth, gaps or discrepancies in the level of the dentition, asymmetry of the dental arch, presence of intraoral lacerations, broken or loose teeth, or numbness in the distribution of the mental nerve. An odor is frequently present. Fractured, missing, or dislocated teeth are frequently seen. An “open bite” occurs if the fracture sufficiently dislocates a segment of jaw so that the teeth cannot be brought into occlusion (Fig. 22.46). The open bite may occur anteriorly, laterally, or bilaterally. On opening, the jaw may deviate toward one side because of the fractures in the subcondylar area, which prevent the balancing effect of the lateral pterygoid muscle. Fractures in the condylar and subcondylar area may result in a laceration of the ear canal that produces bleeding, confusing the injury with that of a middle cranial fossa fracture. Instability of the alveolar section of the mandible relative to the mandibular body implies the presence of an alveolar fracture. Separation of the alveolus from the basilar bone of the mandible creates dramatic dental instability.

FIGURE 22.46 “Open bite” after mandibular fracture treatment. The front teeth cannot be brought into full occlusion because displaced posterior aspects of the mandible block its full motion and alignment with the maxillary teeth.

The mandible has strong muscular attachments that contribute to displacement after injury. The direction of the fracture line may oppose fracture displacement produced by the muscles. The Panorex radiograph uses a rotating x-ray tube to obtain a circumferential view for an excellent evaluation of the entire mandible in a single plane. Lateral oblique, posteroanterior, and Towne’s skull views are used to demonstrate the mandible on plain films. A CT scan provides one of the most accurate evaluations of a mandibular fracture but can occasionally miss nondisplaced fractures. CT scans also demonstrate the course of the fracture through the bone, which is essential for treatment planning.

Management

The treatment of mandibular fractures depends on the state of the dentition and the location of the fracture. It begins with closure of intraoral and extraoral lacerations and the application of arch bars and intermaxillary fixation to bring the teeth into occlusion (Fig. 22.47). In some cases, an acrylic splint can be applied to the teeth temporarily to align them. Some fractures are treated with intermaxillary fixation alone for 4 to 6 weeks after “closed reduction.” For displaced fractures in both the horizontal and vertical portions of the mandible, direct open reduction of the fracture with plate and screw fixation is the preferred treatment. A plate is placed along the inferior border of the mandible, avoiding the mental nerve and tooth roots (Fig. 22.48). At least two screws are placed to each side of the fracture in stable bone.