In 1975 Nahum1 presented the forces necessary to fracture various bones in the facial skeleton. The forces required to fracture the frontal bone were three times greater than those required to fracture the zygoma, maxilla, or mandible. The force required was 800β1600 pounds for the frontal sinus versus 300β750 pounds for the mandibular angle, 550β900 pounds for the mandibular symphysis, 200β400 pounds for the zygomatic arch, and 150β300 pounds for the maxilla. Frontal bone fractures therefore illustrate the high-energy trauma that has occurred and are likely to be associated with other coexisting injuries.
Significant facial fractures, especially those involving the midface, can be associated with uncontrolled hemorrhage, airway compromise, and intracranial and C-spine injury. Each of these elements must be assessed and managed at initial presentation as part of the advanced life support protocol. The internal maxillary artery is the most common source of bleeding in facial fractures although skin or mucosal tears and bone can all cause bleeding that is challenging to control. Uncontrolled bleeding in these cases should be initially managed with posterior nasal packing followed by early fracture reduction. Angiography and selective embolization are normally only recommended once a patient has been stabilized. If a patient is hemodynamically unstable, ligation of the external carotid artery or urgent embolization may be indicated. Neither ligation or embolization risk ischemia to the ipsilateral facial structures because of the considerable overlapping arterial networks in the head and neck.1β4
The focal point of frontal sinus drainage is commonly the osteomeatal complex, which comprises the maxillary, frontal, and anterior ethmoid ostia and is located in the middle meatus.1 Drainage is usually through the nasofrontal ducts into the middle meatus, but this can occur directly. There is some evidence that the frontal sinus may have an independent drainage pattern in some patients. The frontal sinus does not develop until after birth. Development begins at about age 2, and it typically reaches adult size after age 12. It may be visible radiographically from age 8 onward.
4. Bynoe RP, Kerwin AJ, Parker HH III, et al. Maxillofacial injuries and life-threatening hemorrhage: treatment with tran- scatheter arterial embolization. J Trauma 2003;55(1):74β79
with significant displacement of the posterior wall (more than one width of the table). A CSF leak is also present. Frontal sinus fractures are high-energy injuries that present with upper-face edema and bruising. There is often a palpable deformity of the frontal bone with paresthesias of the supraorbital and supratrochlear nerves. CSF leak rhinorrhea may occur where dural laceration is present. The globe may be displaced forward and inferiorly. Management of frontal sinuses depends on a number of key factors built into the algorithm shown in Figs. 35.1 and 35.2. These will depend on the skull wall involved, the degree of fracture displacement, the presence or absence of CSF leak, and whether the nasofrontal duct is involved.1,2 Fig. 35.1 Management algorithm for combined anterior and posterior table fracture. CSF, cerebrospinal fluid. (Adapted from Rohrich RJ, Hollier LH. Management of frontal sinus fractures: changing concepts. Clin Plast Surg 19:219, 1992.) COMBINED ANTERIOR/POSTERIOR TABLE FRACTURE Displaced posterior wall No (<1 table width) CSF leak CSF leak Nasofrontal duct involved No No operative intervention Allow 4-7 days for resolution. If persistent, consider cranialization 1. Reduction/ stabilization of anterior wall 2. Sinus preservation 1. Reduction/ stabilization of anterior wall 2. Cranialization 1. Reduction/ stabilization of anterior wall 2. Sinus obliteration with spontaneous osteogenesis with or without tissue graft Yes No Yes No Yes Yes (>1 table width)
Although access is commonly through a bicoronal approach, access through existing lacerations may be used. Subgaleal dissection is performed to preserve a pericranial flap in case the sinus requires obliteration or cranialization. Obliteration of the sinus may be achieved with bone or fat grafts as alternatives to a pericranial flap, but bone cement should not be used because of potential complications from infection. Cranialization not only involves removal of mucosa and obliteration of the ducts, but also includes removal of the posterior table. The nasal cavity is isolated from the cranial cavity by interposing a pericranial flap, and the anterior table is then reconstructed.1,2
Nasoethmoidal fractures are complex to manage and are associated with changes in postinjury facial appearance due to their involvement of the nasal dorsum, nasoorbital valley, and medial canthus. Use of either bolsters or thermoplastic nasal splints postoperatively is advised to help optimize soft tissue outcomes. Nasoethmoidal fractures have been classified by Markowitz into three groups according to the involvement of a central bony fragment.1 The relevance of this is that the central fragment is the site of attachment of the medial canthal tendon. Disruption of this tendon results in telecanthus. Type I fractures do not involve telecanthus as they represent simple fractures of the central fragment without disruption of the canthal tendon. In type II fractures, there is comminution of the central fragment, but the tendon is not disrupted and may or may not involve telecanthus. Type III fractures involve severe comminution and disruption of the medial canthal tendon. These will display telecanthus. Treatment involves either a direct or bicoronal approach and stabilization requires a combination of Fig. 35.2 Management algorithm for anterior table fracture. (Adapted from Rohrich RJ, Hollier LH. Management of frontal sinus fractures: changing concepts. Clin Plast Surg 19:219, 1992.) No Yes No Displaced No operative intervention Reduction/stabilization with sinus preservation Reduction/stabilization and then sinus obliteration with spontaneous osteogenesis with or without tissue graft Nasofrontal duct involved ANTERIOR TABLE FRACTURE Yes plates, wires, and bone graft. In children, bone grafts are avoided where possible and these patients are at high risk of growth disturbances, given that the septum is a major growth center.2,3
Isolated nasal fractures are the most common fracture of the facial skeleton and early accurate management is essential to minimize long-term deformity and morbidity. The key to achieving good long-term outcomes is to ensure accurate reduction of both the nasal bones and septum in the acute period. Manipulation should therefore be performed in a controlled environment to ensure accuracy of reduction, particularly as in this case where the septum is disrupted. Therefore, a general anesthetic is advised. Where there is minimal swelling as in this case, the reduction is best performed as soon as possible. If there is significant swelling, then elevation and ice should be used, and the patient reassessed in 3β5 days. Imaging is not required for isolated nasal bone fractures. A CT scan, however, is warranted in cases of suspected nasoorbital ethmoid (NOE) fractures or other head injury. Open rhinoplasty is reserved for cases with residual problems after manipulation under anesthesia. Rohrich and Adams1 describe an algorithm for the management of nasal fractures which may be a useful guide in clinical practice. Fractures are classified from I through V, where I through III represents isolated nasal bone fractures, type IV has additional septal disruption (as in this case), and type V corresponds to NOE fractures. Septal fractures (type IV injuries) may require specific attention with reduction, with or without reconstruction/ resection. Septal hematomas are associated with type IVa injuries and require early intervention to avoid necrosis to the septum.1
The orbit consists of seven bones that also include the maxilla and zygoma. The thinnest area is the lamina papyracea, and this is part of the ethmoid. It is so named as it is paper thin. Isolated fractures of the orbital floor and medial wall may occur (without associated fracture of the orbital rim) and these are postulated to occur either from increased pressure that develops within the orbit (from posterior displacement of orbital tissues) or when deformation of the orbital bones occurs from a blow, resulting in fractures of thin portions of the floor without fracture of the orbital rim.1
Enophthalmos and dystopia may occur following an orbital fracture. Enophthalmos is posterior displacement of the globe and occurs either from an increase in the bony orbital volume or a decrease in volume of the globe and surrounding structures. Dystopia refers to a vertical globe malposition. Entrapment of the periocular muscles is rare in adults and is more common in children because of the elastic characteristics of pediatric bone. Entrapment will cause limited eye excursion and diplopia and is a surgical emergency because of potential ischemic muscle damage. Nausea and vomiting in association with pain and limited eye excursion are highly suggestive of entrapment.1,2 Surgical access for orbital fractures is best achieved through subtarsal or transconjunctival approaches. A subciliary approach should be avoided because of a risk of lower eyelid deformity.3,4
The zygoma is an irregular-shaped bone of the skull that forms the lateral cheek and orbital rim. It also contributes to the zygomatic arch, the floor of the orbit, and the infratemporal fossa. The zygoma has four articulations; these are with the frontal, maxilla, sphenoid, and temporal bones. There are left and right zygomas that each comprise the cheek and malar regions. The zygoma is a commonly fractured bone that may be reduced for functional reasons such as correcting enophthalmos or dystopia, eyelid malposition, and trismus. Fractures of the arch are more commonly for cosmetic rather than functional benefits. For example, a fractured zygoma can often result in a flattened appearance to the upper/lateral cheek without any other disability. The exception is when the fracture impedes mandibular excursion by interfering with the coronoid process. When reducing and stabilizing zygoma fractures, it is usual to stabilize three of the articulations.1,2
Although the zygomaticomaxillary complex has four articulations, it is common practice to stabilize just three of these. When treated properly, these fractures do not leave deformities. The AO foundation guidelines recommend that the zygomaticofrontal articulation is plated first, as this allows more control to accurately reduce the remaining articulations.1 It should also ensure the zygomaticosphenoid (not zygomaticotemporal) suture is well aligned and this is the most important to assess. Surgical access will depend on the complexity of the fracture, but a common approach involves intraoral and upper blepharoplasty (not lower) incisions. Wide exposure using a bicoronal approach may be indicated.2,3 The Carroll-Girard screw is a percutaneous T-barβshaped device that can be used as a joystick to reduce and control the fracture.
Rowe forceps are used to facilitate disimpaction of maxillary fractures during surgery. The maxilla contains three vertical and three (not four) horizontal (AP) buttresses. An additional horizontal (AP) buttress is provided by the mandible, not related to the maxilla. Dentoalveolar and LeFort fractures are different. Dentoalveolar fractures pass through the dentition whereas LeFort fractures separate the entire alveolus and dentition from the midface. The fracture line is above the dentition. Malocclusion of the maxilla is commonly seen as an anterior open bite and this is secondary to posteroinferior displacement of the maxilla. LeFort fractures should be reduced and fixed with miniplates and screws through an open approach. Closed reduction and fixation to the mandible are not recommended because this leads to facial lengthening from the downward pull of the mandible.1β3 Treatment considerations for maxillofacial fractures are the same as for adults but may be technically more difficult and some principles in management do differ. For example, arch bars are difficult to place in pediatric patients because of mixed dentition, missing teeth, and unfavorable dental anatomy of the primary teeth. Difficulty can also be encountered in placing fixation systems because of developing tooth buds.4,5
Panfacial fractures involve the upper and midfacial skeleton in association with fractures of the mandible. Management of these injuries is challenging because there is no stable reference from which to begin reduction and stabilization. It may be useful to begin with the mandible to provide a stable base from which to reconstruct the midface. Reconstruction of the zygomas should then be undertaken to provide normal facial projection. Reconstruction then proceeds inferiorly from the stable frontal process to the level of the maxilla. Fixation of the maxilla as a LeFort fracture is the last to be stabilized.1β3
Temporal bone fractures can result in hearing loss, facial nerve paresis, vestibular dysfunction, and CSF leak. Of these, hearing loss is the most common complication, occurring in the vast majority of patients with temporal bone fractures. The risk is related to the fracture configuration with all transverse fractures resulting in hearing loss compared with half of longitudinal fractures. Hearing loss is either sensorineural or conductive. Sensorineural hearing loss does not improve, whereas conductive hearing loss may, unless there is disruption of the ossicular chain. Fracture pattern is also relevant to the risk of developing facial nerve paresis. Loss of facial nerve function is more likely when the fracture pattern is transverse (Table 35.1).1 Vestibular dysfunction can result in vertigo and nystagmus. This has a varied incidence and usually resolves spontaneously once the patient is mobilizing normally. CSF leaks occur in approximately 25% of cases following temporal bone fracture and settle spontaneously within 24 hours. Involvement of the trigeminal nerve is unusual.1,2
Superior orbital fissure syndrome occurs in association with LeFort II/III or zygomatic orbital fractures. It involves the oculomotor, trochlear, abducens, and trigeminal nerves and the ophthalmic vein. It therefore results in the constellation of signs as described above. With reduction of fractures, recovery typically occurs over weeks. Orbital apex syndrome is similar, but also includes a loss of vision, because the optic nerve is involved at the apex.1,2 Traumatic cavernous sinus fistula occurs with arterial bleeding so blood shunts from the internal carotid artery to the cavernous sinus. Signs include proptosis, an ocular bruit, injection, chemosis of the affected eye, and ophthalmoplegia of CN II, IV, or VI. Angiography will provide the diagnosis with evidence of a dilated ophthalmic vein. Fistulas typically close spontaneously. Treatment may include surgical ligation of the carotid artery or placement of coils by an interventional radiologist.3 Traumatic optic neuropathy (TON) is a traumatic loss of vision without external or initial ophthalmoscopic evidence of injury to the eye or the optic nerve. It may occur secondary to globe injury, retinal vascular occlusion, or orbital compartment syndrome. The only objective finding is the presence of a relative afferent pupillary defect.4,5 Sympathetic ophthalmia is a bilateral granulomatous inflammation of the uvea occurring as a complication of penetrating trauma.
There are three ocular emergencies that should have treatment commenced within minutes. They are central retinal artery occlusion, chemical burns, and retrobulbar hematoma. The other injuries listed should be assessed and treated quickly but less urgently. Central retinal artery occlusion is caused by an embolic event, which occludes it. Essentially it is a cerebrovascular incident of the globe and may be transient or permanent depending on the cause and its longevity. Table 35.1 Fracture Patterns and Complications in Temporal Bone Fractures Fracture Pattern Representative Proportion of All Cases Facial Nerve Involvement as a Proportion of Fracture Subtype Hearing Loss as a Proportion of Fracture Subtype Longitudinal 80β90% 20% 67% Transverse 10β20% 40% 100% It is, in theory, a medical emergency yet there is no single proven treatment that will definitely help. For example, thrombolysis, hyperventilation, paracentesis, and ocular massage have all been trialled with no proven success. Often therefore management tends to be focused on prevention rather than cure.1,2 Chemical burns to the eye must be treated swiftly with copious irrigation, ideally commenced at the injury location with more formal treatment on arrival at hospital. Normal saline or water are most often indicated for the irrigation.3 Retrobulbar hematoma is associated with facial trauma and can occur following elective ocular surgery including blepharoplasty. Management is aimed at reducing ocular pressure and often takes the form of surgical decompression of the globe with a lateral canthotomy/cantholysis. Medical management can include oxygen therapy, intravenous mannitol, intravenous acetazolamide, steroids, and topical Ξ²-blockers.4,5 Corneal abrasions are treated conservatively. They usually re-epithelialize in 24 hours. Traumatic mydriasis is pupillary sphincter rupture resulting in a permanently dilated pupil. This is also treated nonoperatively. Hyphema is blood in the anterior eye chamber. This is treated by prevention of a rebleed, bed rest, and atropine to decrease iris movement.
Diagnosis of CSF leak in patients following head injury is based on clinical examination of the nose and external ear, backed up by CT scanning or laboratory tests. Beta transferrin is a carbohydrate-free form of transferrin, which is almost exclusively found in the CSF. Beta transferrin is not present in blood, nasal mucus, tears, or mucosal discharge, so is specific to CSF even where the fluid is bloodstained and difficult to assess clinically. It has been shown to have a sensitivity of near 100% and a specificity of about 95% for CSF leak in a large retrospective study.1 Detection of glucose in the sample fluid using Glucostix test strips is another traditional test for CSF in nasal and ear discharge but is not recommended as a confirmatory test because of its lack of specificity and sensitivity.2 Interpretation of the results is confounded by various factors such as contamination from glucose-containing fluid (tears, nasal mucus, blood in nasal mucus) or relatively low CSF glucose levels. The other tests listed do not relate to CSF leak tests. Albumin and prealbumin are used as markers of nutritional state.
Maxillary fractures may be classified using the LeFort system. There are three types of LeFort fracture as shown in Fig. 35.3, A through C. They differ in their extent. A LeFort I (Fig. 35.3, A) separates the tooth-bearing maxilla from the midface. It extends from the piriform aperture posteriorly through the nasal septum, lateral nasal walls, and maxillary wall through the maxillary tuberosity or pterygoid plates. The LeFort II (Fig. 35.3, B) is a pyramidal fracture that extends through the frontonasal junction along the medial orbital wall, usually passing through the inferior orbital rim at the zygomaticomaxillary (ZM) suture. It continues posteriorly through the pterygoid plates. It leaves the upper jaw and nasal bones as a mobile solitary unit. The LeFort III (Fig. 35.3, C) fracture represents craniofacial disjunction extending through the frontonasal junction along the medial orbital wall and inferior orbital fissure and out the lateral orbital wall. Dentoalveolar fractures involve the teeth and supporting osseous structures only.1
A Gillies maneuver is an approach to elevate a zygomatic arch fracture through a temporal hairline incision. The elevator is passed beneath the deep temporal fascia under the arch and the arch is elevated, taking care not to lever against the underlying temporal bone (Fig. 35.4). Fig. 35.3 LeFort midfacial fractures. A, LeFort I fracture separating the inferior portion of the maxilla in horizontal fashion, extending from the piriform aperture of the nose to the pterygoid maxillary suture area. B, LeFort II fracture involving separation of the maxilla and nasal complex from the cranial base, zygomatic orbital rim area, and pterygoid maxillary suture area. C, LeFort III fracture (i.e., craniofacial separation) is complete separation of the midface at the level of the nasoorbital ethmoid (NOE) complex and zygomaticomaxillary (ZM) suture area. It extends through the orbits bilaterally. A B C Fig. 35.4 Reduction maneuvers for an isolated zygomatic arch fracture. A, The Gillies approach involves a 2-cm incision placed 2 fingerbreadths above the helix and 2 fingerbreadths anterior. A blunt elevator is placed beneath the deep layer of deep temporal fascia, superficial to the temporalis muscle allowing the tip of the elevator to pass behind the arch without risking injury to the frontal branch of the facial nerve. B, In the intraoral approach (Keen), a 1- to 2-cm incision is made laterally in the buccal sulcus. Subperiosteal elevation allows the elevator to be placed behind the arch. A B An alternative approach as described by Keen involves a 1- to 2-cm incision made lateral to the buccal sulcus. Subperiosteal elevation allows the elevator to be placed behind the arch.1
pattern? This patient has Battleβs sign, which is ecchymosis over the mastoid process and seen in conjunction with a skull base fracture. It is associated with temporal bone fractures but is not exclusive to them. For example, it is also seen in fractures of the occipital, sphenoid, and ethmoid bones. Battleβs sign typically appears 2β3 days following injury and may be associated with other signs of skull base fracture such as otorrhea, rhinorrhea, facial nerve palsy, nystagmus, hemotympanum, and deafness. Raccoon eyes may also be present, which are black patches in the periorbital region secondary to ecchymosis.1,2
Sympathetic ophthalmia is a rare bilateral granulomatous inflammation of the uvea. It occurs as a consequence of penetrating trauma or a surgical insult to a single eye. The nontraumatized eye typically becomes inflamed within 1 year of injury, and a severely traumatized eye may be best treated early with enucleation early to prevent this. An alternative approach to treatment involves the use of immunosuppressive medical therapy. This may include locally injected or systemic steroids and infliximab. The precise pathophysiology is not known although recent developments in molecular biology and imaging technology are proving useful in elucidating the autoimmune processes involved.1,2 Vitreous hemorrhage is a condition where bleeding occurs within the vitreous humor of the globe. It can be secondary to trauma and associated with retinal detachment. Presenting signs and symptoms vary according to severity. In smaller bleeds patients may describe floaters, cobwebs, haze, or shadows in the eye. The most severe bleeds can cause complete visual loss. Traumatic optic neuropathy (TON) presents with loss of vision following trauma, without external or initial ophthalmoscopic evidence of injury to the eye or the optic nerve. It may occur secondary to globe injury, retinal vascular occlusion, or orbital compartment syndrome. The only objective finding is the presence of a relative afferent pupillary defect. Iridodialysis describes a traumatic separation between the iris root and ciliary body. It may be caused by nonpenetrating or penetrating trauma to the globe. Clinical features include pain and blurred vision. Orbital apex syndrome occurs in association with some midface or zygomatic orbital fractures. It involves the oculomotor, trochlear, abducens, and trigeminal nerves and the ophthalmic vein. It therefore results in a constellation of signs in keeping with damage to these nerves. It can lead to complete loss of vision because the optic nerve is involved at the apex.3,4