Craniofacial Injuries

Published on 13/03/2015 by admin

Filed under Neurosurgery

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 2045 times

CHAPTER 339 Craniofacial Injuries

The craniofacial region extends from the coronal suture to the chin. The bony and soft tissue anatomy includes the anterior portion of the skull vault and base, the facial skeleton, and the soft tissue coverings. The viscera include the frontal lobes of the brain, the contents of the orbit, associated cranial nerves, the upper airway, and the upper digestive tract.

Injuries to this anatomically and functionally complex region require the skills of several disciplines and are best managed in a multidisciplinary manner, if not by a formal multidisciplinary team. It follows that the management of craniofacial injuries should be integrated into a regional trauma service that is capable of providing lifesaving emergency and specialist care for extracranial injuries and has a workload sufficient to maintain the skills needed for multidisciplinary assessment and all the disciplines necessary for the treatment of craniofacial injuries in the short and long term.

Epidemiology

The causes of craniofacial trauma reflect the general pattern of neurotrauma but with significant regional variations. Worldwide, modes of transportation are the main cause of neurotrauma and craniofacial trauma. In high-income countries, an overall fall in transport injuries, the use of air bags in motor vehicles, and the use of helmets by motorcyclists have reduced the incidence of maxillofacial injury. Falls in infancy and old age and pedestrian and bicycle accidents have become major causes in some countries.1 There remains a high incidence in motorbike riders, particularly adolescents. Facial fractures are more common with open face helmets, and the most severe injuries occur in riders with no helmet.2 Furthermore, with the development of efficient retrieval systems, more patients with severe injuries survive to reach trauma centers. In developing countries, the continuing rise in the incidence of transport-related neurotrauma3 and the corresponding rise in severe head injuries are accompanied by a parallel increase in craniofacial injury, although these figures are not well documented.

Other causes of craniofacial trauma include falls, assaults,4,5 sporting injuries, industrial accidents, and missile injuries.1,2,6,7

Severe craniofacial fractures, typified by panfacial fracture involving all regions of the face, are most often associated with motor vehicle accidents. In this group, major injuries to other systems are common.8

In organizing multidisciplinary care and planning preventive strategies, an understanding of the causes and incidences in a particular community is essential.4,5,9

Functional Anatomy

The Anterior Cranium

The anterior cranial fossa is formed anteriorly and laterally by the frontal bones. The frontal bones are attached to the facial skeleton by the frontonasal, frontomaxillary, and frontozygomatic sutures. The floor of the anterior cranial fossa constitutes the interface between the cranium and the facial skeleton. It is formed laterally by thin supraorbital plates that dip down medially to articulate via the frontoethmoidal sutures with the cribriform plates and crista galli, parts of the ethmoid bone, and posteriorly with the lesser wings of the sphenoid bone via the sphenofrontal sutures. The cribriform plates may be quite narrow and are the lowest points of the anterior fossa floor, on average located 8 mm below the nasion. They form part of the roof of the nose and are related laterally to the anterior and middle ethmoid air cells.

Posteriorly, the ethmoid bone attaches to the body of the sphenoid, which is the roof of the sphenoid sinuses. Laterally, the lesser wings of the sphenoid form the crescentic posterior borders of the anterior fossa. The optic canal is formed by the two roots of the lesser wing of the sphenoid and runs forward and laterally in the superolateral wall of the sphenoid sinus to the orbital apex.10

The temporal bone forms part of the cranial base. The squamous part articulates with the mandible at the temporomandibular joint.

Fractures of the anterior fossa floor may involve the frontal, ethmoid, or sphenoid sinuses; the cribriform plates; or laterally, the optic canals. In making extradural approaches to this region via a frontal craniotomy, access is greatly increased by removing a bar of bone that includes the supraorbital margins and transects the frontal sinuses.

The complex sphenoid bone is the keystone for the craniofacial skeleton; it contributes to the middle cranial fossa, the anterior cranial fossa, the lateral orbital wall, and the subtemporal fossa.

The Paranasal Air Sinuses

The size and degree of pneumatization of the paranasal air sinuses (Fig. 339-1) are variable. At birth all the sinuses are rudimentary and do not reach adult proportions until puberty (see Chapter 341).8

Pathophysiology

Optic Nerve

Traumatic injury to the optic nerve is indicated by a dilated, sometimes irregular pupil with hippus; the pupil does not show a direct or consensual light reaction but does react to contralateral light. With a partial injury, some light reactions may be seen.13 Flash evoked potentials may help diagnose early injury in unconscious patients and children.14

The optic nerve may be compressed by a displaced fracture through the optic canal, by contusion or hematoma within the canal without a fracture, or by direct injury to the orbit.15,16

The Globe and Orbit

The orbit may be fractured directly or indirectly as part of frontal, nasoethmoid, midface, or zygomatic fractures. Orbital fractures may be indicated by diplopia, enophthalmos, impaired globe elevation because of entrapment of soft tissues, and paresthesia of the cheek or upper incisor teeth. The orbital signs may become apparent only after the edema has subsided.

Early marked exophthalmos suggests a significant reduction in bony orbital volume and requires urgent ophthalmologic and radiologic examination.

Orbital wall fractures may be “blow-out” or “blow-in” (outward on inward buckling of the orbital wall). A pure blow-in or blow-out fracture is one in which the orbital rim is intact; those often inaccurately referred to as “impure” fractures are extensions of fractures involving the orbital rim. Isolated medial wall defects in the middle third of the orbit increase orbital volume posterior to the axis of the globe and may cause enophthalmos. Until the advent of computed tomography (CT), these fractures were not easily recognized.

The globe can be injured by direct penetration or by blunt force. The globe is robust and cushioned by the surrounding soft tissue and will resist a blunt force sufficient to cause a blow-out fracture of the floor or medial wall.17 Nonetheless, the incidence of ocular injury with an orbital fracture is about 20%.18 Blunt injuries to the globe include corneal abrasions, hyphema, vitreous hemorrhage, and retinal detachment.

Penetration injury may damage any part of the globe and cause immediate or delayed loss of vision. The patient’s visual acuity is the best guide to the likelihood of visual recovery. If there is no perception of light, recovery of useful vision is highly unlikely.

Clinical examination may show chemosis, subconjunctival swelling, and poor visual acuity. During preoperative assessment it is important to avoid causing additional damage by placing pressure on the globe.

Mechanisms of Injury

Initial Management

Severe craniofacial injuries often pose an immediate threat to life. Airway obstruction caused by massive shattering of the facial skeleton, dislodged dentures, or collapse of the mandibular arch with retrodisplacement of the tongue may result in severe hypoxia.

There may be profuse bleeding, hypovolemic shock, and hypotension. They are often associated with injuries elsewhere in the body. Consequently, less severe craniofacial injuries may be overlooked in the urgency to manage severe injuries elsewhere in the body.21

Specific Acute Problems with Craniofacial Injuries

Breathing

Breathing may be impaired by head or chest injuries. Cough and swallowing reflexes may be impaired both by the direct injury and by brain injury.

Clinical Assessment

The Face

Bruising, lacerations, and contour deformities should be noted and recorded. Periorbital bruising (raccoon eyes) indicates a possible anterior fossa fracture. The mastoid region may show bruising (Battle’s sign) from a temporal bone fracture.

CSF leakage should be sought, although it may be hard to identify with certainty in the presence of blood and mucus. Secretion of saliva in the wounds may indicate injury to the salivary glands. Jaw movements and the muscles of facial expression are tested. The cervical spine is palpated for tenderness or deformity and the scalp for lacerations and hematomas.

By standing behind the patient with the head held back, any asymmetry of the facial prominences or deviations from the midline will be apparent.

Each facial region should be palpated systematically from the frontal bone to the mandible to specifically seek evidence of deformity or abnormal movement. Palpation of the inferior orbital margin may help differentiate isolated fractures of the zygoma (where the lateral part of the inferior rim is usually depressed) from midface pyramidal fractures or nasomaxillary fractures (where the medial aspect of the rim is depressed).

The mandible is examined with the patient’s mouth slightly open; the posterior rami, angles, lower border, and symphyseal regions are first palpated externally. Condylar movements are palpated by placing an examining finger in the external auditory meatus with the pulp directed anteriorly during active mandibular excursions. An intraoral examination is performed with a gloved finger to palpate the alveolar ridges and the hard palate. Dentoalveolar injuries are recorded on a dental chart. The anterior wall of the maxilla and the zygomaticomaxillary junctions are also palpated intraorally. Abnormal movements of the midface are elicited by grasping the maxillary alveolar ridge or pressing on the anterior hard palate (but not the incisor teeth) and applying a rocking movement while palpating the face with the free hand.

Abnormalities in dental occlusion must be noted.

Investigations

Later Imaging

In general, detailed diagnostic imaging of the craniofacial injury should not be performed until a full clinical examination has been completed and a plan of investigation has been formulated. The principle investigation is CT.

Standard Radiographic Projections

Management

Brain Injury

Craniocerebral injuries may be classified into five main clinical groups:

At all stages of care the possibility of a primary brain injury needs to be kept in mind and steps taken to minimize the risk for secondary injury:

Orbital Injury

Optic Nerve Injury

Management of traumatic optic nerve injury remains controversial, and the debate whether observation alone is better than steroids, surgical decompression, or a combination of the two remains unresolved.2936 A regimen of megadose methylprednisolone (loading dose of up to 30 mg/kg; maintenance dose of up to 5 mg/kg per hour for 72 hours) followed by a gradual reduction has been recommended37; however, the International Optic Nerve Trauma Study found no benefit from either corticosteroid therapy or optic nerve decompression.32 A Cochrane review published in 2005 noted a high rate of spontaneous recovery and concluded that traumatic optic nerve injury initially seen more than 8 hours after injury should not be treated with steroids; for those seen within 8 hours, the evidence of benefit was weak.38 Several papers have reported some good results after endoscopic decompression.33,39,40 A small study reported better results in those operated early30; however, a further Cochrane review in 2007 was unable to find sufficient evidence from the small retrospective series available and noted the risk for complications.41

Definitive Repair

Once the necessary assessments have been completed, a treatment plan is devised by all the specialties involved. Isolated injuries rarely give rise to conflicting treatment priorities, whereas multiple injuries and complex craniofacial injuries require a clear assessment of priorities based on the degrees of urgency.

In deciding on the appropriateness of early versus delayed surgery,4244 the following principles need to be observed:

Surgical Principles

There are three important anatomic sites of injury to the craniofacial interface.

Craniofacial Exposures

Surgical treatment is typically based on wide exposure of the craniofacial skeleton via a bicoronal scalp flap or periorbital, intraoral, and extraoral incisions. Recently, endoscopy has been used for some orbital fractures, for fractures of the mandibular condyles, and for repair of anterior cranial base fractures with CSF rhinorrhea (see Chapter 341).

The Bicoronal Scalp Flap

This flap is placed behind the patient’s hairline when possible. The incision may be a straight line from ear to ear, as is usual in neurosurgery, or a wavy or zigzag line, which gives a better cosmetic result (Fig. 339-3). The flap is raised in a subgaleal plane to 2 to 4 cm above the supraorbital rim or the site of any fractures of the frontal bone. From this level the dissection proceeds subpericranially over the orbital rim and into the orbit. The supraorbital neurovascular bundle is carefully preserved, if necessary by fracturing the margins of the supraorbital notch with a fine osteotome.

It is important to dissect strictly against the temporal fascia or to incise through the superficial layer of the temporal fascia and dissect at the subfascial fat plane down to the zygomatic arch to preserve the frontal branch of the facial nerve, which lies superficially within or above the superficial temporal fascia. At the level of the zygomatic arch the periosteum is stripped with great care, particularly from the middle and posterior thirds. This may be difficult when the arch is fractured, and the frontalis branch of the facial nerve can be damaged. Within the orbit the periorbita is dissected to within 1 cm of the apex. When orbital fractures are present, soft tissue may be trapped between bony fragments, which must be separated to release the soft tissue. The temporomandibular joint and the neck of the condyle can be approached by extending the bicoronal flap to the lobule of the ear. Careful dissection of the soft tissue from the lateral ligaments of the temporomandibular joint capsule enables visualization of the neck of the condyle and the sigmoid notch. Further access can be gained by dividing the most posterior fibers of the masseter muscle, and the subperiosteal dissection can be taken down to the angle of the mandible.

Subciliary lower eyelid incisions or transconjunctival incisions with or without a lateral canthotomy provide excellent exposure of the orbital floor.46

Intraoral incisions in the upper and lower buccal sulci provide exposure of the remaining facial skeleton with the exception of the pterygoid plate. Care must be taken to avoid damage to branches of the infraorbital nerve by the upper buccal sulcus incision and the inferior dental nerve by the lower buccal sulcus incision. In an edentulous mandible the inferior dental nerve is very superficial intraorally, and in such cases an external mandibular incision is preferable.

Bone Grafting

After severe injuries bone is often missing from one or more of the vertical bony pillars of the midface.43 The thin bone of the floor and medial wall of the orbit may be lost with orbital fractures.

Bone grafting is sometimes needed to reconstruct defects in the orbital rim or to correct the nasal bridge line after severe comminution of the nasal bones and bony nasal septum. Gunshot wounds may result in significant loss of bone. When this loss is greater than 3 cm in length, vascularized bone provides more certain healing.

Common donor sites for harvesting bone are the iliac crest, rib cage and skull vault (calvaria). Many factors are important for the survival of bone grafts, the most important being rigid fixation followed by good soft tissue coverage, preferably with a periosteal surface.47 Other factors include a well-vascularized bed in the host tissues and prevention of hematoma formation.

Internal fixation is achieved with small plates and screws constructed of materials such as titanium, which is biologically inert and compatible with MRI.

Titanium mesh and other alloplastic materials can be used to reconstruct the orbits, although bone is preferable. Absorbable plates and screws have been developed and are undergoing trial for use in traumatic injuries.

Donor Sites

Calvarial Grafts

Calvarial bone has the disadvantage of being more rigid than either iliac bone or rib. The outer table can be safely split from the skull at sites where there is a well-formed diploic space (Fig. 339-4), as is usual in the parietal area; however, radiographs must be examined to determine whether the skull is thick enough to perform the maneuver safely. The sagittal sinus and its parasagittal venous tributaries must be avoided, and great care should be taken to avoid penetrating the dura mater. When a small square of bone is needed, as for the orbital floor, the pericranium can be left attached to prevent fragmentation of the graft. Contour defects are hard to avoid when the outer table is harvested. The inner table can be harvested when a craniotomy is being performed and the calvaria is thick enough.

Specific Fracture Patterns

Fractures Involving the Frontal Sinus

A compound depressed fracture of the frontal sinus involving the anterior and posterior walls is best approached through a bicoronal scalp flap (Figs. 339-5 and 339-6). A small frontal craniotomy is made above the sinus area to expose the posterior wall of the sinus, and the depressed fracture is approached extradurally. If the dura is torn, the posterior wall of the frontal sinus is drilled away and the sinus mucosa stripped. The dura is repaired in a watertight manner by primary suture or by patching with a graft of temporal fascia or pericranium placed intradurally if possible. The sinus ostia can be plugged with muscle. A pericranial graft attached inferiorly is turned forward and sutured to the dura to seal the frontal sinus. If soft tissue injuries prevent such grafting, a free graft of temporal fascia can be laid over the exposed frontal sinus and sutured to the dura and to the pericranium. The technique is designed to obliterate the sinus. The anterior wall of the frontal sinus is preserved. If it is comminuted, the fragments are wired or plated in good position.48

Central depressed fractures of the frontal region may be associated with orbitoethmoid fractures and fractures of the floor of the anterior cranial fossa, often complicated by CSF rhinorrhea. This constellation of injuries is best managed by a combined operation in which the fractures are elevated and fixed with miniplates and the anterior fossa is explored intradurally and repaired if the disruption is severe and the degree of brain swelling is not prohibitive.

A closed depressed fracture of the anterior wall of an extensive frontal sinus without damage to the posterior wall may be reconstructed with small wires or microplates.

Closed anterior and posterior wall fractures with CSF leakage are observed, and if the leak persists beyond 1 week, dural repair is performed.

A simple posterior wall fracture without a dural fistula need not be treated.

Naso-orbito-ethmoid Fractures

These injuries result from a direct impact to the midface, with the primary point of contact being at the nasal complex. High-energy impacts cause fractures that extend posteriorly into the delicate ethmoid bone, superiorly into the frontal sinus, inferiorly into the nasal septum, and laterally into the orbital floor. The anterior fossa floor may be fractured. The central unstable bone fragments include the attachment of the medial canthal ligaments. These in turn are part of the eyelid suspensory ligaments and surround the lacrimal sac.

These fractures may be unilateral or bilateral, simple or comminuted, closed or compound. They may occur in isolation or in association with more extensive fracturing of the forehead, orbit, or maxilla.49

The characteristic deformity is best seen in lateral profile. Collapse of the nasal pyramid results in posterior displacement of the nasal dorsum and upward tilting of the nasal tip. When viewed from the front, flattening and spreading of the intercanthal region are observed.

Ophthalmologic examination is essential to exclude associated injuries to the globe and adnexa. Neurosurgical evaluation is necessary because of the potential for an anterior fossa dural tear and cranionasal fistula.

Operative Management

Nasoethmoid fractures are treated by open reduction and interfragmentary fixation with screws. If necessary, primary bone grafts are applied to the medial orbital walls and nasal dorsum, and the medial canthal ligaments are reattached.50,51

A bicoronal scalp incision and subperiosteal dissection are performed to expose the orbital roof, medial orbital walls, nasal bones, and frontal processes of the maxillae. Care must be taken to preserve any attachment of the medial canthal ligaments. Conjunctival or subciliary incisions are made to expose the orbital floor. Upper buccal sulcus incisions give access to the nasomaxillary buttresses. Limited access may be obtained through nasofrontal lacerations.

If the naso-orbito-ethmoid complex is fractured as a single segment, the block can be reduced and fixed with microplate and screw fixation at two points. The canthal attachments remain intact and the canthal relationships are not disturbed. When the injury is more severe and fragmentation extends into the medial orbital wall, reconstruction proceeds from posterior to anterior. Bone grafts are applied to the medial orbital wall and the fragments fixed with miniplates or microplates. A transnasal canthopexy is performed in which transnasal 28-gauge wires are passed through the canthal ligaments and then posterior and superior to the lacrimal fossa. In severe cases, a primary bone or costochondral graft placed as a cantilever restores the nasal bridge and maintains the soft tissue by preventing scar contracture, which makes secondary surgery very difficult. The graft is fixed superiorly by plates and screws or by screw fixation alone. The distal portion is inserted under the lower lateral nasal cartilage to maintain nasal tip position. The nasal septum is invariably buckled and is best managed at this stage by gentle closed manipulation, with definitive correction left for a later time.

Fractures of the Zygoma

The zygomatic bone forms part of the lateral wall and floor of the orbit and makes an essential contribution to orbital contour and facial width and projection.52

Zygomatic fractures may be indicated by swelling, bruising, subconjunctival hemorrhage (particularly laterally), double vision, or blurred vision. Numbness or altered sensation commonly occurs in the distribution of the infraorbital nerve. Trismus and complaints of malocclusion indicate that the arch fractures are impinging on the underlying temporalis muscle.

Palpation will readily identify displacement. The inferior orbital rim may exhibit a palpable “step-down” on palpating in a medial-to-lateral direction. When the zygomatic fracture is associated with extensive midfacial fracturing, the zygomatic arch is bowed outward and the anteroposterior projection of the zygomatic prominence is diminished. Intraoral examination will show bruising in the upper vestibule.

Detailed ophthalmologic examination is essential.

Coronal CT scans show the orbital walls and the floor. Axial views show the deformation of the zygomatic body, arch, and lateral and medial orbital walls.

Treatment

An undisplaced zygomatic fracture requires no operative intervention.

An isolated, displaced zygomatic arch fracture is usually treated by closed reduction.53

Orbitozygomatic fractures require careful open reduction and internal miniplate fixation. Wide operative exposure of the orbitozygomatic skeleton allows anatomic restoration of the zygomatic prominence with fewer positional disturbances of the globe, such as enophthalmos and vertical dystopia. Because the masseter muscle is the major displacing force acting on the zygoma, miniplate fixation of the zygomaticomaxillary buttress and the zygomaticofrontal articulation should orientate the vertices of fixation in the optimal axis.

If there is significant comminution at the zygomaticomaxillary buttress, it may be necessary to bone-graft the resultant gap after reduction has been achieved.

Comminuted and grossly displaced orbitozygomatic fractures are almost always caused by high-velocity impacts and are associated with major midface or panfacial fractures. Gruss and colleagues advised first restoring the anterior projection of the zygomatic arch because this is key to restoring facial projection.52 The zygomatic arch is the significant reference point with respect to midfacial width and anteroposterior projection in panfacial fractures. CT will indicate the possibility of loss of bone in the orbital floor. In severe fractures, the medial orbital wall can be damaged as well, and bone grafting may be necessary in both these sites to restore orbital volume. The orbital wall components of zygomatic fractures do not require exploration if CT shows no displacement.

Orbital Injury

High-resolution axial CT scans with bone and soft tissue windows will show the medial and lateral walls and extension of fractures into the cranial base, zygoma, and midface. Coronal views will show the orbital roof, medial and lateral walls, and orbital floor.

When a pure blow-out fracture is suspected, direct coronal scans of the orbit will accurately identify the extent of involvement of the floor and medial wall and the nature of the soft tissue abnormality.

Hematomas may also be identified. Comparison with the contralateral orbit on an axial CT scan provides qualitative assessment of the degree of enophthalmos; quantification of posttraumatic enophthalmos and the changes produced by surgical correction are revealed by comparison of precorrection and postcorrection CT scans.

Management of orbital injury aims to accurately restore first the orbital rim and then the walls to return the globe to its preinjury position with full ocular motility. This should be done early to prevent the development of soft tissue fibrotic changes. The orbital rim is reduced and fixed internally with microplates or miniplates, and the orbital walls are reconstructed with primary bone grafts if comminuted or bone loss is extensive.

The floor is approached through a transconjunctival incision or subciliary lower eyelid incision (Figs. 339-7 and 339-8).

The lateral wall may be approached through an eyebrow incision, and the medial wall, roof, and lateral walls can be approached via a bicoronal scalp flap. Fractures of the medial orbital wall have been approached endoscopically through incisions in the medial canthal region. The dissection is in the subperiosteal plane. Herniated soft tissues are replaced in the orbit when possible and the defects repaired.

In small isolated blow-out fractures of the orbital floor, the displaced bony fragment may be elevated and allowed to override. In the majority of cases, however, this is inadequate and correction requires orbital wall reconstruction. The materials used can be either autogenous bone or cartilage grafts or alloplastic implants, absorbable or nonabsorbable. Titanium mesh has very suitable biocompatibility and can be used to restore the orbital cavity contours in complex facial fractures because it can be shaped accurately. It is best used in combination with autogenous bone grafts. Autogenous bone on its own is the best material for orbital repair, provided that the grafts are adequately shaped, placed anatomically, and fixed when possible. They are less prone to infection or extrusion. Bone grafts may be calvarial, rib, or hip. For the medial orbital wall, a thinned portion of the inner table of the ilium shaped to replace the eggshell-like lateral wall of the ethmoid is introduced via the bicoronal scalp flap and subperiorbital dissection.

The most common complication is enophthalmos, which is often due to inadequate exposure of the full extent of the bony defect, particularly a medial orbital wall fracture. Ocular and canthal dystopia results from inaccurate reduction of the zygoma and failure to maintain the bony attachments of the medial canthus and restore the lateral canthal region.54 There may be damage to the globe or impaired motility from scarring or tethering.

Fractures of the Mandible

Fractures of the mandible are relevant to craniofacial surgery as an important component of panfacial fractures. Correct realignment of the mandible is mandatory for rebuilding the maxilla and the orbits to restore correct facial proportions (Fig. 339-9).

Stable fractures without displacement are best treated conservatively.

A displaced fracture of the body or angle of the mandible in an adult usually requires reduction and stabilization for 6 weeks. Any displaced fracture through a tooth root is inevitably compound. Fractures of the ramus and condylar region are not compound unless caused by a penetrating agent.

An orthopantogram gives an excellent view of the angles and coronoid and condylar processes. A CT scan may give useful information regarding the integrity of the buccal and lingual plates.

In patients with a displaced fracture, dental impressions are taken to provide plaster casts of occlusion in the position resulting from injury. These casts are then cut at the fracture site and mounted on an articulator in the predicted pretraumatic position so that they can be used as models in planning management.

Maxillary Fracture Patterns

Maxillary fractures are still most often classified according to the original description by Le Fort (Fig. 339-10), although fractures rarely conform to this pattern and more detailed and accurate descriptions are now based on CT scanning.55

Management

Conservative management is undertaken in the following two situations:

Displaced upper jaw fractures require open reduction and internal fixation.43

Preoperative dental impressions of the dental arch are used to cast a plaster model. The pretrauma occlusion is determined and an acrylic bite wafer constructed on the dental cast. This is used perioperatively and often postoperatively to maintain the correct occlusion.

Because upper jaw fractures may compromise both the oral and nasal cavities, preoperative airway management needs careful planning.

After careful disimpaction and mobilization of the fractures, an acrylic occlusal wafer is wired to the upper jaw. The jaw is placed in occlusion and stabilized with intermaxillary wires. The relationship of the upper jaw to the midface buttresses is established with the mandibular condyles properly seated in the glenoid fossae. Fixation is achieved through the four anterior vertical midface buttresses. If any of these buttresses is comminuted, vertical height can be maintained with bone grafting. After all four buttresses are stabilized with miniplates or bone grafting, the intermaxillary fixation may be released and the success of the reduction confirmed by seeing the lower teeth engage cleanly into the wafer. The fracture is then supported with one or two very light elastic bands between the upper and lower jaws.

Different sequences must be considered when the bones of the upper midface are also fractured and when there is a simultaneous mandibular fracture.57

When the upper jaw fracture is associated with displaced orbital fractures, particularly the zygomatic or naso-orbital component, these are first stabilized. The occlusal complex, which consists of the upper and lower jaws united, is then brought up to the stabilized upper midface, and the final fixation, with or without bone grafting, is carried out along the lines of the buttresses (Fig. 339-11).

Postoperatively, the intermaxillary fixation is released early. The acrylic occlusal wafer may be left on the upper jaw and the mandible permitted to engage in the dental facets on the inferior aspect of the wafer for a number of days. Light rubber band traction may be placed between the upper and lower jaws in the premolar region after the first 24 hours to inhibit contraction of the medial pterygoid muscles during the earlier stages of mobilization. Patients are nursed while sitting up as soon as possible to reduce facial swelling, and jaw mobilization is commenced almost immediately.

Multiple and Panfacial Fractures

Severe impact to the central part of the face may damage all regions to varying degrees (Fig. 339-12). Because the fracture patterns are extremely variable, there is no standard approach to management. Repair requires repositioning existing bone, replacing severely comminuted or lost bone with primary autogenous bone grafts, and replacing or expanding craniofacial soft tissues to the pretraumatic state.

The first step in management is to restore midface projection and width in relation to the cranial base and mandible.

Gruss and associates grouped these complex injuries into three broad anatomic divisions43:

In most cases there are three key anatomic sites of injury:

Treatment

Complex craniofacial fractures ideally require definitive correction of the bony injuries within the first 5 to 7 days. As noted earlier, some aim for primary fixation within 12 to 48 hours of injury, but this early time frame may not allow adequate preoperative radiologic, ophthalmologic, and dental assessment, especially when the patient is comatose or poorly cooperative. During this early phase, soft tissue swelling makes operative exposure and assessment of facial projection and symmetry difficult. CSF rhinorrhea or an intracranial aerocele may provide additional reasons for delay to determine whether dural repair is necessary.

When early acute neurosurgical intervention is necessary for intracranial clots or compound calvarial fractures, the scalp incisions should be designed to allow later exposure and stabilization of the craniofacial fractures. Because fixation of a mobile face requires an intact fronto-orbital bar, a frontal bone flap elevated to expose the anterior cranial fossa must be positioned to maintain the stable superior points for fixation. When treating a depressed fracture of the temporal region, it may be possible to stabilize fractures extending into the lateral orbital wall and greater wing of the sphenoid. Indeed, delayed repair of an orbital fracture may risk displacing a previously corrected cranial component and causing intracranial bleeding or dural injury.

Sequence of Repair

The sequence of repair depends on the status of the boundaries of the injured face—the calvarial vault above and the mandible below.58

When the frontal cranium is intact, there is fracturing but no loss of bone in the anterior cranial fossa or fronto-orbital bar, or these structures have already been rigidly fixed at a previous operation, the orbitozygomatic and midfacial regions can be built from above downward. The key steps in this sequence are proper positioning and fixation of the zygomatic arches.

There are other situations in which repair proceeds from below upward. If the mandibular arch is disrupted, especially if it is foreshortened as a result of fracture or fracture-dislocation of the condylar processes, it should be repaired initially to establish a solid basis and posterior facial height. Once the mandible is rigidly restored, the midface can be disimpacted and placed in the predicted occlusion. Intermaxillary fixation is then instituted. Repair subsequently proceeds from above down to meet the already fixed maxillary-mandibular segment. Miniplate fixation or bone grafting is used to reconstitute the four anterior buttresses (Fig. 339-13).

Repair also proceeds from below upward if there has been cranial bone loss and disruption of the floor of the anterior cranial fossa such that the superior reference points have been lost or distorted. The mandible and midface are repaired first, and this reconstituted complex is reattached to the cranium above after any necessary anterior fossa dural repair has been performed.

Sagittal Fractures of the Midface

Vertical fractures through the alveolar process and palate occur in 24% of Le Fort fractures, and 78% are associated with mandibular fractures.59 They require careful presurgical dental modeling, sequential repair as outlined, and on occasion, open fixation of the hard palate fracture.

Infancy and Childhood

The skeleton and dentition in children are evolving entities. Development of the skeleton and soft tissues is interrelated and dependent on the functional status of the matrix on which the tissues are growing. Both trauma and surgical intervention can interfere with the growth processes in ways that may not be apparent until years later.60,61

The incidence of facial fractures is lower in childhood and particularly in infancy. Reasons given for this lower incidence are

The most common causes of injury are falls in play or sports.4,61

Pediatric injuries in motor vehicle accidents often result from severe impact, and associated injuries have been reported in more than 60% of children.60,63

The patterns of injury are different from those seen in adults. The calvaria is more prominent in early life and therefore more exposed to injury. The frontal bone in infancy is a thin plate of woven bone and can become indented (a “ping-pong” fracture). There is a greater risk for contrecoup contusions with frontal impact because of the thinner skull.

As the calvarial bone thickens and becomes more resistant to injury, linear and depressed fractures can occur, frequently with fracture lines extending into the orbit.

The facial skeleton at birth contains relatively more cancellous bone and cartilage than the adult facial skeleton. It contains all the unerupted teeth and has not yet been weakened by development of the paranasal sinuses. This accounts for the resilience of the infant’s mandible and midfacial complex to impact. Greenstick fractures are more common. Before completion of eruption of the permanent dentition (5 to 12 years), the presence of unerupted teeth predisposes the bones of the midface and mandible to more oblique and sagittal fractures through the developing tooth crypts.64

The most common facial fractures in childhood are nasal and mandibular.65,66 Isolated fractures of the midface are rare. Orbital roof fractures may be overlooked and should be considered if there is evidence of injury about the eye.67,68

By 7 years, orbitocranial growth is very nearly completed. After the age of 12 years, sinus aeration is near completion, adult dentition is established, and mineralization of the skeleton becomes complete. The facial skeleton has changed from a solid resilient mass to a complex system of robust but rigid pillars and thin plates. The fracture patterns therefore become those of the adult.12

Soft Tissue Injury

Soft tissue injuries should be closed as soon as possible; however, in multiply injured patients requiring urgent stabilization or surgery, closure can be delayed for up to 48 hours. If delay is necessary, the wounds should be cleaned, irrigated with normal saline to remove as much foreign material as possible, and covered with a sterile dressing. Antibiotics are given only for gross contamination.

Definitive closure can usually be performed under local anesthesia. Copious irrigation, careful inspection for foreign material, minimal débridement, and precise anatomic suturing are required.

Puncture Wounds

Puncture wounds can be deceptive, with the depth and direction of penetration not being clear from superficial examination.72 Deeply situated vital structures may be injured. The penetrating object is not usually sterile, and the distal part may break off. The wound should be carefully explored with a blunt instrument. Radiography or CT may show embedded matter. MRI may be necessary to identify wood or glass fragments. Penetration near a major vessel may require angiography.

Wounds near the upper eyelid, especially in children, should be treated with caution because an object such as pencil or chopstick can quite easily penetrate the thin orbital roof,73 yet there may be little or no external signs of penetration. Careful neurological and neuro-ophthalmologic assessment should be undertaken, and if deep penetration is suspected, scanning should be performed to identify the bony defect and the track. Retained wood fragments should be removed because they present a risk of infection. Penetration by metal objects may be treated with antibiotics alone.

Complications

Dural Fistula

Fractures of the midface (Le Fort I and II) and nasoethmoid fractures may lead to cranionasal fistulas through the cribriform plates and frontal, ethmoid, or sphenoid sinuses.74 CSF rhinorrhea should be searched for in all patients who may have an anterior fossa fracture and confirmed by β2-transferrin testing. It has been estimated that 35% of patients with severe facial fractures have a CSF fistula and that 60% will cease within 10 days. This may be assisted by accurate reduction of the facial fractures. If the leak persists beyond 10 days, surgical treatment may be necessary (see Chapter 341).

Vascular Injury

Severe frontal impact may result in vascular injury that is often not apparent or overlooked in the early assessments.76,77 Such injuries include carotid cavernous fistulas and carotid or vertebral artery dissection, thrombosis, or aneurysm.

Carotid-Cavernous Fistulas

The most common cause of carotid cavernous fistulas is head trauma, usually blunt and less often penetrating.78 They occur in approximately 1% of patients with facial fractures.79 The internal carotid artery is vulnerable to shearing forces acting between the fixed points of attachment at its dural entry and exit to the cavernous sinus. The fistula may result from a tear in the artery itself or from a tear in meningeal branches of the internal carotid or external carotid arteries within the cavernous sinus. Traumatic fistulas are most often due to a single tear in the internal carotid artery and are high flow. The visual symptoms and signs are chiefly due to the elevated venous pressure. Flow in the superior and inferior ophthalmic veins is frequently reversed, with engorgement and dilation of these vessels. High venous pressure causes chemosis, proptosis, and elevated intraocular pressure and glaucoma; venous distention may also cause paralysis of the third, fourth, and sixth cranial nerves. There is often a latent interval between injury and the signs of a fistula. In such cases, it is considered likely that a minor tear in the internal carotid artery gave rise to a traumatic aneurysm and that delayed rupture of the aneurysm led to the fistula. A few patients suffer cerebral ischemia from diversion of arterial blood into the fistula (steal effect),80 especially if the circle of Willis is markedly asymmetric.81 Nontraumatic fistulas are more often due to tears in meningeal branches and are low flow.

Internal Carotid Artery Injury

The intracranial internal carotid artery may be injured in association with fractures through the petrous temporal bone within the carotid canal or by fractures at the anterior clinoid process.76,8286 The onset of ischemic symptoms is immediate in a third of patients and occurs within 24 hours in a third. Treatment is generally conservative. Some have suggested extracranial/intracranial bypass for bilateral injuries. Traumatic aneurysms of the supraclinoid internal carotid artery have also been reported.87

Suggested Readings

Chen CT, Huang F, Tsay PK, et al. Endoscopically assisted transconjunctival decompression of traumatic optic neuropathy. J Craniofac Surg. 2007;18:19.

Cooter RD, David DJ. Computer-based coding of fractures in the craniofacial region. Br J Plast Surg. 1989;42:17.

Crompton J, Hammerton M. Ocular injuries. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:397.

David DJ. Exploration of the orbital floor through a conjunctival approach. Aust N Z J Surg. 1974;44:25.

Gassner R, Tuli T, Hachl O, et al. Craniomaxillofacial trauma in children: a review of 3,385 cases with 6,060 injuries in 10 years. J Oral Maxillofac Surg. 2004;62:399.

Gruss JS. Complex craniomaxillofacial trauma: evolving concepts in management. A trauma unit’s experience—1989 Fraser B. Gurd lecture. J Trauma. 1990;30:377.

Gruss JS. Fronto-naso-orbital trauma. Clin Plast Surg. 1982;9:577.

Gruss JS, Antonyshyn O, Phillips JH. Early definitive bone and soft-tissue reconstruction of major gunshot wounds of the face. Plast Reconstr Surg. 1991;87:436.

Hanieh A, Moore MH. Immaturity and senescence. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:501.

Hemmy DC, David DJ, Herman GT. Three-dimensional reconstruction of craniofacial deformity using computed tomography. Neurosurgery. 1983;13:534.

Leipziger LS, Manson PN. Nasoethmoid orbital fractures. Current concepts and management principles. Clin Plast Surg. 1992;19:167.

Liebenberg WA, Demetriades AK, Hankins M, et al. Penetrating civilian craniocerebral gunshot wounds: a protocol of delayed surgery. Neurosurgery. 2005;57:293.

Lo YL, Yang TC, Liao CC, et al. Diagnosis of traumatic internal carotid artery injury: the role of craniofacial fracture. J Craniofac Surg. 2007;18:361.

Markowitz BL, Manson PN. Panfacial fractures: organization of treatment. Clin Plast Surg. 1989;16:105.

McKinney A, Ott F, Short J, et al. Angiographic frequency of blunt cerebrovascular injury in patients with carotid canal or vertebral foramen fractures on multidetector CT. Eur J Radiol. 2007;62:385.

Moore MH, David DJ, Cooter RD. Oblique craniofacial fractures in children. J Craniofac Surg. 1990;1:4.

Shenaq SM, Wildberger JE. Maxillofacial and scalp injury in neurotrauma. In: Narayan RK, Dinh T, Povlishock JT, editors. Neurotrauma. New York: McGraw Hill; 1996:225.

Simpson DA, Abbott J. Pathology of injury and repair. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:119.

Singh DJ, Bartlett SP. Pediatric craniofacial fractures: long-term consequences. Clin Plast Surg. 2004;31:499.

Smoot EC3rd, Jernigan JR, Kinsley E, et al. A survey of operative airway management practices for midface fractures. J Craniofac Surg. 1997;8:201.

Trott JA, David D. Definitive management: principles, priorities and basic techniques. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:233.

Yu-Wai-Man P, Griffiths PG. Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev. 4, 2007. CD006032

Yu Wai Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev. 4, 2005. CD005024

References

1 Iida S, Hassfeld S, Reuther T, et al. Maxillofacial fractures resulting from falls. J Craniomaxillofac Surg. 2003;31:278.

2 Rocchi G, Fadda MT, Marianetti TM, et al. Craniofacial trauma in adolescents: incidence, etiology, and prevention. J Trauma. 2007;62:404.

3 Akama MK, Chindia ML, Macigo FG, et al. Pattern of maxillofacial and associated injuries in road traffic accidents. East Afr Med J. 2007;84:287.

4 Eggensperger Wymann NM, Holzle A, Zachariou Z, et al. Pediatric craniofacial trauma. J Oral Maxillofac Surg. 2008;66:58.

5 Kontio R, Suuronen R, Ponkkonen H, et al. Have the causes of maxillofacial fractures changed over the last 16 years in Finland? An epidemiological study of 725 fractures. Dent Traumatol. 2005;21:14.

6 Ong TK, Dudley M. Craniofacial trauma presenting at an adult accident and emergency department with an emphasis on soft tissue injuries. Injury. 1999;30:357.

7 Taher AA. Management of weapon injuries to the craniofacial skeleton. J Craniofac Surg. 1998;9:371.

8 Follmar KE, Debruijn M, Baccarani A, et al. Concomitant injuries in patients with panfacial fractures. J Trauma. 2007;63:831.

9 Fasola AO, Nyako EA, Obiechina AE, et al. Trends in the characteristics of maxillofacial fractures in Nigeria. J Oral Maxillofac Surg. 2003;61:1140.

10 DeLano MC, Fun FY, Zinreich SJ. Relationship of the optic nerve to the posterior paranasal sinuses: a CT anatomic study. AJNR Am J Neuroradiol. 1996;17:669.

11 Rudderman RH, Mullen RL. Biomechanics of the facial skeleton. Clin Plast Surg. 1992;19:11.

12 Caldicott WJ, North JB, Simpson DA. Traumatic cerebrospinal fluid fistulas in children. J Neurosurg. 1973;38:1.

13 Simpson DA. Clinical examination and grading. In: Reilly PL, Bullak R, editors. Head Injury: Pathophysiology and Management. 2nd ed. London: Hodder Arnold; 2005:143.

14 Cornelius CP, Altenmuller E, Ehrenfeld M. The use of flash visual evoked potentials in the early diagnosis of suspected optic nerve lesions due to craniofacial trauma. J Craniomaxillofac Surg. 1996;24:1.

15 Nayak SR, Kirtane MV, Ingle MV. Fracture line in post head injury optic nerve damage. J Laryngol Otol. 1991;105:203.

16 Stonecipher KG, Conway MD, Karcioglu ZA, et al. Hematoma of the optic nerve sheath after penetrating trauma. South Med J. 1990;83:1230.

17 Converse J, Smith B. Orbital and naso-frontal fractures. et al. Converse J, editor. Reconstructive Plastic Surgery: Principles and Procedures in Correction, Reconstruction and Transplantation, 2nd ed, Philadelphia: WB Saunders, 1977.

18 Barry C, Coyle M, Idrees Z, et al. Ocular findings in patients with orbitozygomatic complex fractures: a retrospective study. J Oral Maxillofac Surg. 2008;66:888.

19 Liebenberg WA, Demetriades AK, Hankins M, et al. Penetrating civilian craniocerebral gunshot wounds: a protocol of delayed surgery. Neurosurgery. 2005;57:293.

20 Ahmad F, Kirkpatrick NA, Lyne J, et al. Buckling and hydraulic mechanisms in orbital blowout fractures: fact or fiction? J Craniofac Surg. 2006;17:438.

21 Katzen JT, Jarrahy R, Eby JB, et al. Craniofacial and skull base trauma. J Trauma. 2003;54:1026.

22 Smoot EC3rd, Jernigan JR, Kinsley E, et al. A survey of operative airway management practices for midface fractures. J Craniofac Surg. 1997;8:201.

23 Hemmy DC, David DJ, Herman GT. Three-dimensional reconstruction of craniofacial deformity using computed tomography. Neurosurgery. 1983;13:534.

24 Gillespie JE, Isherwood I, Barker GR, et al. Three-dimensional reformations of computed tomography in the assessment of facial trauma. Clin Radiol. 1987;38:523.

25 Levy RA, Edwards WT, Meyer JR, et al. Facial trauma and 3-D reconstructive imaging: insufficiencies and correctives. AJNR Am J Neuroradiol. 1992;13:885.

26 Zinreich SJ. 3-D reconstruction for evaluation of facial trauma. AJNR Am J Neuroradiol. 1992;13:893.

27 Crompton J, Hammerton M. Ocular injuries. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:397.

28 Specht CS, Varga JH, Jalali MM, et al. Orbitocranial wooden foreign body diagnosed by magnetic resonance imaging. Dry wood can be isodense with air and orbital fat by computed tomography. Surv Ophthalmol. 1992;36:341.

29 Girard BC, Bouzas EA, Lamas G, et al. Visual improvement after transethmoid-sphenoid decompression in optic nerve injuries. J Clin Neuroophthalmol. 1992;12:142.

30 Gupta AK, Gupta AK, Gupta A, et al. Traumatic optic neuropathy in pediatric population: early intervention or delayed intervention? Int J Pediatr Otorhinolaryngol. 2007;71:559.

31 Guy J, Sherwood M, Day AL. Surgical treatment of progressive visual loss in traumatic optic neuropathy. Report of two cases. J Neurosurg. 1989;70:799.

32 Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy: the International Optic Nerve Trauma Study. Ophthalmology. 1999;106:1268.

33 Li KK, Teknos TN, Lai A, et al. Extracranial optic nerve decompression: a 10-year review of 92 patients. J Craniofac Surg. 1999;10:454.

34 Mahapatra AK. Does optic nerve injury require decompression? J Indian Med Assoc. 1990;88:82.

35 Schroder M, Kolenda H, Loibnegger E, et al. [Optic nerve damage following craniocerebral trauma. A critical analysis of trans-ethmoid decompression of the optic nerve.]. Laryngorhinootologie. 1989;68:534.

36 Spoor TC, Hartel WC, Lensink DB, et al. Treatment of traumatic optic neuropathy with corticosteroids. Am J Ophthalmol. 1990;110:665.

37 Cepela MA, George CE. Orbital trauma. Curr Opin Ophthalmol. 1997;8:64.

38 Yu-Wai-Man P, Griffiths PG. Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev. 2007;4:CD006032.

39 Chen CT, Huang F, Tsay PK, et al. Endoscopically assisted transconjunctival decompression of traumatic optic neuropathy. J Craniofac Surg. 2007;18:19.

40 Li HB, Shi JB, Cheng L, et al. Salvage optic nerve decompression for traumatic blindness under nasal endoscopy: risk and benefit analysis. Clin Otolaryngol. 2007;32:447.

41 Yu Wai Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev. 2005;4:CD005024.

42 Becelli R, Renzi G, Perugini M, et al. Craniofacial traumas: immediate and delayed treatment. J Craniofac Surg. 2000;11:265.

43 Gruss JS, Phillips JH. Complex facial trauma: the evolving role of rigid fixation and immediate bone graft reconstruction. Clin Plast Surg. 1989;16:93.

44 Gruss JS, Pollock RA, Phillips JH, et al. Combined injuries of the cranium and face. Br J Plast Surg. 1989;42:385.

45 Gruss JS. Complex craniomaxillofacial trauma: evolving concepts in management. A trauma unit’s experience—1989 Fraser B. Gurd lecture. J Trauma. 1990;30:377.

46 David DJ. Exploration of the orbital floor through a conjunctival approach. Aust N Z J Surg. 1974;44:25.

47 Rahn BA. Theoretical considerations in rigid fixation of facial bones. Clin Plast Surg. 1989;16:21.

48 Rohrich RJ, Hollier LH. Management of frontal sinus fractures. Changing concepts. Clin Plast Surg. 1992;19:219.

49 Gruss JS. Fronto-naso-orbital trauma. Clin Plast Surg. 1982;9:577.

50 Leipziger LS, Manson PN. Nasoethmoid orbital fractures. Current concepts and management principles. Clin Plast Surg. 1992;19:167.

51 Trott JA, David D. Definitive management: principles, priorities and basic techniques. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:233.

52 Gruss JS, Van Wyck L, Phillips JH, et al. The importance of the zygomatic arch in complex midfacial fracture repair and correction of posttraumatic orbitozygomatic deformities. Plast Reconstr Surg. 1990;85:878.

53 Gillies HD, Kilner TP, Stone D. Fractures of the malar-zygomatic compound, with description of a new x-ray position. Br J Surg. 1927;14:651.

54 Wolfe SA. Treatment of post-traumatic orbital deformities. Clin Plast Surg. 1988;15:225.

55 Cooter RD, David DJ. Computer-based coding of fractures in the craniofacial region. Br J Plast Surg. 1989;42:17.

56 Thaller SR, Kawamoto HK. A histologic evaluation of fracture repair in the midface. Plast Reconstr Surg. 1990;85:196.

57 Markowitz BL, Manson PN. Panfacial fractures: organization of treatment. Clin Plast Surg. 1989;16:105.

58 Shenaq SM, Dinh T. Maxillofacial and scalp injury in neurotrauma. In: Narayan RK, Wildberger JE, Povlishock JT, editors. Neurotrauma. New York: McGraw Hill; 1996:225.

59 Antoniades K, Dimitriou C, Triaridis C, et al. Sagittal fracture of the maxilla. J Craniomaxillofac Surg. 1990;18:260.

60 Hanieh A, Moore MH. Immaturity and senescence. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:501.

61 Singh DJ, Bartlett SP. Pediatric craniofacial fractures: long-term consequences. Clin Plast Surg. 2004;31:499.

62 Gassner R, Tuli T, Hachl O, et al. Craniomaxillofacial trauma in children: a review of 3,385 cases with 6,060 injuries in 10 years. J Oral Maxillofac Surg. 2004;62:399.

63 Ferreira PC, Amarante JM, Silva PN, et al. Retrospective study of 1251 maxillofacial fractures in children and adolescents. Plast Reconstr Surg. 2005;115:1500.

64 Moore MH, David DJ, Cooter RD. Oblique craniofacial fractures in children. J Craniofac Surg. 1990;1:4.

65 Kaban LB, Mulliken JB, Murray JE. Facial fractures in children: an analysis of 122 fractures in 109 patients. Plast Reconstr Surg. 1977;59:15.

66 McCoy FJ, Chandler RA, Crow ML. Facial fractures in children. Plast Reconstr Surg. 1966;37:209.

67 Clauser L, Dallera V, Sarti E, et al. Frontobasilar fractures in children. Childs Nerv Syst. 2004;20:168.

68 Greenwald MJ, Boston D, Pensler JM, et al. Orbital roof fractures in childhood. Ophthalmology. 1989;96:491.

69 Ousterhout DK, Vargervik K. Maxillary hypoplasia secondary to midfacial trauma in childhood. Plast Reconstr Surg. 1987;80:491.

70 Gruss JS, Antonyshyn O, Phillips JH. Early definitive bone and soft-tissue reconstruction of major gunshot wounds of the face. Plast Reconstr Surg. 1991;87:436.

71 Tan E. Injuries of Soft Tissues, Ducts and Nerves. Edinburgh: Churchill Livingstone; 1995.

72 Balasubramanian C, Kaliaperumal C, Jadun CK, et al. Transorbital intracranial penetrating injury—an anatomical classification. Surg Neurol. 2009;71:238-240.

73 Park SH, Cho KH, Shin YS, et al. Penetrating craniofacial injuries in children with wooden and metal chopsticks. Pediatr Neurosurg. 2006;42:138.

74 Morgan BD, Madan DK, Bergerot JP. Fractures of the middle third of the face—a review of 300 cases. Br J Plast Surg. 1972;25:147.

75 Simpson DA, Abbott J. Pathology of injury and repair. In: David DJ, Simpson DA, editors. Craniomaxillofacial Trauma. Edinburgh: Churchill Livingstone; 1995:119.

76 Lo YL, Yang TC, Liao CC, et al. Diagnosis of traumatic internal carotid artery injury: the role of craniofacial fracture. J Craniofac Surg. 2007;18:361.

77 McKinney A, Ott F, Short J, et al. Angiographic frequency of blunt cerebrovascular injury in patients with carotid canal or vertebral foramen fractures on multidetector CT. Eur J Radiol. 2007;62:385.

78 Gratz KW, Imhof HG, Valavanis A. Traumatic carotid cavernous sinus fistula due to a gun shot injury. Int J Oral Maxillofac Surg. 1991;20:280.

79 Chang CJ, Chen YR, Noordhoff MS, et al. Facial bone fracture associated with carotid-cavernous sinus fistula. J Trauma. 1990;30:1335.

80 Watanabe A, Ishii R, Suzuki Y, et al. The cerebral circulation in cases of carotid cavernous fistula. Findings of single photon emission computed tomography. Neuroradiology. 1990;32:108.

81 Iida K, Uozumi T, Arita K, et al. Steal phenomenon in a traumatic carotid-cavernous fistula. J Trauma. 1995;39:1015.

82 Ajir F, Tibbetts JC. Post-traumatic occlusion of the supraclinoid internal carotid artery. Neurosurgery. 1981;9:173.

83 Carter DA, Mehelas TJ, Savolaine ER, et al. Basal skull fracture with traumatic polycranial neuropathy and occluded left carotid artery: significance of fractures along the course of the carotid artery. J Trauma. 1998;44:230.

84 Morgan MK, Besser M, Johnston I, et al. Intracranial carotid artery injury in closed head trauma. J Neurosurg. 1987;66:192.

85 Yang TC, Lo YL, Huang YC, et al. Traumatic anterior cerebral artery aneurysm following blunt craniofacial trauma. Eur Neurol. 2007;58:239.

86 York G, Barboriak D, Petrella J, et al. Association of internal carotid artery injury with carotid canal fractures in patients with head trauma. AJR Am J Roentgenol. 2005;184:1672.

87 Pozzati E, Gaist G, Servadei F. Traumatic aneurysms of the supraclinoid internal carotid artery. J Neurosurg. 1982;57:418.

88 Ferreras J, Junquera LM, Garcia-Consuegra L. Intracranial placement of a nasogastric tube after severe craniofacial trauma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2000;90:564.

89 Wood MM, Reilly PL, David DJ. Neuropsychologic outcome after craniofacial fracture. J Craniofac Surg. 1990;1:163.

90 Jimenez DF, Sundrani S, Barone CM. Posttraumatic anosmia in craniofacial trauma. J Craniomaxillofac Trauma. 1997;3:8.