Management of Skull Base Trauma

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Chapter 136 Management of Skull Base Trauma

Skull base trauma encompasses injury to the neurovascular and bony elements of the orbital plate of the frontal bone, the cribriform plate of the ethmoid bone, the sphenoid bone, the squamous and petrous temporal bone, and the suboccipital bone. Biomechanical studies have shown that the skull base is surprisingly elastic. Strong ligaments within the skull base and tough connective tissue in the suture lines are resilient and often may not be disrupted by the forceful impact. However, fractures within the bony elements of the skull base occur in approximately 25% of all blunt head injuries.1 A basilar skull fracture does not necessarily imply that the site of impact was to the skull base. Severe forces anywhere to the cranium can radiate down and disrupt the bony integrity of the base of skull.2 Most commonly, skull base fractures result from direct trauma either to the frontal and supraorbital regions or to the occiput. Cranial nerve and major arterial and venous injuries are more common in traumatic brain injury (TBI) accompanied by a skull base fracture.3

Graft Repair Options

A variety of graft options are available for surgical repair of skull base defects. Autologous grafts are preferred and include vascularized pericranium and rotational flaps of temporalis muscle and fascia. Nonvascularized, free grafts of pericranium, temporalis, rectus femoris, and abdominal muscle or fascia lata can also be used. Vascularized pedicle grafts resist infection and incorporate more quickly into the recipient site than free flaps, and they give a watertight seal that is durable for years.5,6 In the setting of trauma, defects in the pericranium are common and repair techniques have been described to salvage these grafts.7 The dura of the anterior falx can also be used to close dural defects.8 The accessibility of vascularized, septal mucosal flaps is a valuable adjunct to skull base repairs during endoscopic approaches.9 Dead space invites infection, and the presence of viable tissue in the vicinity chosen for graft placement is important to facilitate graft survival. Fat may be used to fill large defects and is preferred over nonvascularized muscle, which can fibrose and atrophy. While fat is preferred over muscle for its longer durability, free fat grafts rely on their ability to parasitize blood supply from adjacent soft tissue, and they may resorb when juxtaposed to devitalized bone and dura.10,11

Large bone defects from comminuted fractures in the skull base are best repaired using the patient’s own bone. Large fracture fragments may be debrided, soaked in antibiotic solution, and reapproximated with a titanium craniofacial plating system. Reconstruction by plating of multiple small fragments and of the thin bones of the nose and orbit is not recommended, because it carries significant risk of bony resorption of the repair. Fracture defects in the orbital roof should always be reconstructed, either with titanium mesh or with a synthetic prosthesis, to prevent pulsatile exophthalmos. Split calvarium is preferred for autologous repair when large defects cannot be primarily reconstructed with the fracture fragments. Bone can also be harvested from iliac crest and rib. Calvaria bone has a low resorption rate (17%-19%), whereas the rate of resorption for iliac crest and rib may approach 60% to 80%.1215 Use of oblique angles in the bone cuts can reduce the number of screws and plates required for reapproximation of the bone flap. Septal cartilage can also be used for reconstruction of the ethmoid and sphenoid skull base. Inorganic implants, including both titanium mesh and porous, polyethylene implants, yield excellent cosmetic results for reconstruction of soft tissue and bony defects with a low risk of complications.16 However, methyl methacrylate and other cranioplasty cements should not be used to repair fracture defects, because they do not give a watertight seal and are predisposed to entrapping microbes leading to delayed infectious complications, especially when placed in the vicinity of the paranasal sinuses. Use of monocryl suture, an absorbable copolymer of glycolide and caprolactone, minimizes tissue reaction during healing and slowly hydrolyses over a period of 3 to 4 months.

Skull Base Fractures

Clinical signs of skull base fracture include anosmia, bilateral periorbital ecchymosis, hemotympanum and/or perforation of the tympanic membrane, facial palsy, hearing loss, nystagmus, vertigo, cerebrospinal fluid (CSF) rhinorrhea or otorrhea, and ecchymosis over the mastoid prominence, also known as a Battle sign.17,18 Techniques of surgical repair of associated facial, mandibular, and orbital fractures that frequently accompany skull base fractures are beyond the scope of this review. CSF leaks occur in 10% to 20% of skull base fractures.8,1921 The proximity of basilar skull fractures to the paranasal sinuses raises concern for meningitis if the dura is torn in the vicinity of the fracture. Prophylactic antibiotics do not decrease the incidence of meningitis in basilar skull fractures2225; rather, they may predispose the patient to a higher risk of superinfection with resistant organisms.26,27 The risk of meningitis persists even years after the trauma, independent of whether or not the patient developed a CSF fistula with the injury.28,29

Anterior Skull Base Fractures


Anterior skull base fractures of the orbital and cribriform plates frequently extend to involve the frontal sinus. Frontal sinus fractures may be open or closed and displaced or nondisplaced. In 40% to 60% of cases, both walls of the sinus are fractured, although isolated fractures of either the anterior or, less commonly, the posterior wall may occur.3032 There is a 15% to 30% incidence of CSF leak associated with frontal sinus fractures.33 In particular, anterior wall fractures that extend into the base of the anterior fossa or those involving the posterior sinus wall should be observed closely for CSF leak. Fractures of the anterior skull base are an absolute contraindication to passage of a nasogastric feeding tube or nasopharyngeal airway.34

Obstruction of the nasofrontal outflow tracts is common, occurring in approximately 70% of frontal sinus fractures.32 These tracts connect the frontal and ethmoid sinuses, and the status of their patency is a key criterion for surgical intervention.32,3538 Indirect signs of nasofrontal outflow obstruction include computed tomography (CT) evidence of fluid in the frontal sinus and fractures of the medial frontal sinus floor.3941 Nasoethmoidal or supraorbital fractures, especially those medial to the supraorbital notch, raise suspicion for nasofrontal outflow obstruction.42,43 Facial fractures, most commonly orbital floor, naso-orbitoethmoidal complex, zygomatic, and Le Fort fractures are three times more likely in patients with nasofrontal outflow tract involvement.32 Complications of missed outflow obstruction include chronic sinusitis and mucocele formation.4447 Mucoceles have a high likelihood of becoming infected, thereby giving rise to frontal osteomyelitis or Pott’s puffy tumor, in addition to epidural and subdural empyemas.

Operative indications for frontal sinus fractures include (1) anterior table displacement with cosmetic deformity; (2) fractures with evidence of nasofrontal outflow obstruction; (3) displacement of the posterior table greater than the thickness of the skull, because this predicts likely dural laceration; and (4) presence of refractory CSF leak.32,36,42 Closed, depressed anterior wall fractures frequently cause cosmetic deformity and may require surgical repair for cosmesis. Some have argued that fractures that do not involve the nasofrontal outflow tract are rarely displaced enough to require cosmetic realignment.32 The management of posterior wall frontal sinus fractures is complex and varied.4851 Extensive comminution of the posterior sinus wall,52 fracture dislocation greater than the width of the posterior table,36,44 or accompanying CSF leak48,53 is an indication for surgical repair. Rodriguez et al.32 suggest that, as for anterior frontal sinus fractures, posterior frontal wall fractures with nasofrontal outflow obstruction should undergo surgical repair with either obliteration or cranialization of the frontal sinus. In their series of 31 nondisplaced posterior wall fractures, they had 3 complications following conservative management, and all 3 occurred in patients with nasofrontal outflow obstruction.32 In patients managed conservatively, a follow-up CT should be considered to check that there is no residual fluid level and that the frontal sinus is draining normally.


Repair options for frontal sinus fractures include reconstruction, obliteration, and cranialization.32,51,54 Simple reconstruction involves in situ elevation and plating of the sinus wall fracture with preservation of the nasofrontal ducts and sinus mucosa. Fractures that impair the nasofrontal duct should be treated by obliteration or cranialization procedures in which the frontal sinus mucosa is removed completely and the nasofrontal ducts are blocked. The frontal sinus is filled and closed off in an obliteration procedure. In a cranialization procedure, the posterior wall of the frontal sinus is removed and the sinus cavity is excluded from the cranial compartment by a pericranial graft.

Reconstruction should be reserved for fractures of the anterior frontal sinus with cosmetic deformity and without signs of nasofrontal duct obstruction (Fig. 136-1). Both endoscopic and open techniques may be employed to reconstruct simple anterior frontal sinus fractures.55,56 Intraoperatively, the patency of the nasofrontal outflow tract can be verified by instilling fluorescein or methylene blue medially at the posterior aspect of the sinus floor and checking for staining of Cottonoids inserted at the level of the middle meatus. Attempts to reconstruct the nasofrontal outflow tract with stents5759 is associated with a high rate of failure due to restenosis and other complications.36,54

Obliteration procedures are employed for complex anterior displaced frontal sinus fractures with obstruction of the nasofrontal outflow tracts. These complex fractures are best approached through a bicoronal scalp incision and bifrontal craniotomy with removal of the sinus mucosa, blockage of the nasofrontal ducts, reduction or fixation of the fracture, and obliteration of the sinus cavity.60,61 The fracture fragments are elevated and stabilized with low-profile craniofacial miniplates. During frontal sinus repair, complete removal of the frontal sinus mucosa is difficult due to the numerous small excrescences of mucosa that line the small cavities and divets within the sinus and follow the paths of the exiting veins of Breschet.62 Drilling 1 to 2 mm of bone from the sinus wall facilitates removal of these small excrescences of mucosa.62 The nasofrontal ducts are blocked with a combination of small pieces of temporalis muscle and small bone chips to prevent ascending infection or mucocele “in growth” from the nasal sinuses. In an obliteration procedure, the sinus cavity is filled with muscle, bone, or alloplasts such as Gelfoam (Pfizer, New York, NY). Bone dust from the cancellous bone of the calvarium resists resorption and facilitates ossification of the sinus.56,63,64 Fat should be avoided if possible. Survival of fat grafts depends on a vascular bed. Especially in the setting of comminuted fractures, there is a high rate of complication (22%) with resorption and fibrous replacement of the fat graft.32 Alloplastic biomaterials such as hydroxyapatite, bioactive glass, methyl methacrylate, calcium phosphate bone cement, and oxidized regenerated cellulose have also been used to obliterate the sinus, but most surgeons advocate autogenous materials.32 If the sinus cavity is not filled, spontaneous obliteration occurs by a process of osteoneogenesis in which scar tissue and bone slowly form and thereby obliterate the sinus cavity. Obliteration of the frontal sinus cavity by the process of osteoneogenesis is associated with a high risk of complications (49%).32

Open depressed fractures of the anterior sinus wall are also often best repaired through a bicoronal scalp incision, because the exposure offered through the traumatic laceration is seldom large enough to enable elevation of the fractured bone fragments, debridement of sinus mucosa, and blockage of the nasofrontal ducts. Fracture fragments from open depressed injuries should be debrided, but they may be incorporated into the reconstruction without increased risk of infection.65,66 Large defects can be repaired using split calvarium. Ideally, open depressed fractures should be repaired within hours of the injury.

Fractures of the posterior sinus wall are generally best repaired by a cranialization procedure through an open craniotomy following the principles for anterior sinus wall fractures. In a cranialization procedure, the posterior sinus wall is removed so that the frontal sinus becomes part of the intracranial cavity (Fig. 136-2). With cranialization, the sinus does not need to be obliterated, a process reliant on the variable survival of fat, muscle, or bone used to obliterate the sinus. The frontal sinus should be cranialized, with removal of the posterior wall of the sinus, if more than 25% of the posterior sinus wall is fractured. However, some reserve cranialization procedures for only the most complex frontal sinus fractures with open depressed injuries and comminuted depressed posterior wall fragments. Cranialization entails expansion of the cranial compartment into the sinus with complete removal of the frontal sinus mucosa and obliteration of the communication to the nasal sinuses. The dura is carefully inspected for lacerations, which are repaired. As for obliteration procedures, the sinus mucosa is completely removed and the nasofrontal ducts are blocked to exclude the intracranial cavity from the nasal sinuses.52,67 A vascularized pericranial graft is harvested, reflected over the preexisting frontal sinus, and tacked to the dura (Fig. 136-3).

Posterior frontal sinus wall fractures that are non-displaced wall fractures can be treated conservatively.36,48 For small posterior sinus wall defects, the frontal sinus can be obliterated with exenteration of the mucosa, blockage of the nasofrontal ducts, and packing of the sinus.20 Removal of a small amount of the posterior wall in the area of the fracture allows exploration and repair of underlying dural lacerations. Reconstruction, rather than cranialization, of the fractured posterior sinus wall has been advocated by some surgeons, but this has not been widely adopted.68,69 Others have suggested that removal of the mucosa is the most important and the nasofrontal ducts do not need to be blocked.70 Leaving the nasofrontal ducts open can only be considered when the surgeon is certain that there is no risk of CSF leak from the sinus fracture. If the nasofrontal ducts are not blocked, there is a risk of delayed mucocele formation, as the mucosal cells of the nasal sinus can migrate up through the duct and repopulate the frontal sinus.32 High rates of complication accompany posterior sinus wall fractures with nasofrontal outflow obstruction that are treated either conservatively or by reconstruction alone, without obliteration of the sinus mucosa and blockage of the nasofrontal ducts; complication rates were 73% for reconstruction and 63% following conservative observation.32 By comparison, overall complications rates for repair of frontal sinus fractures with nasofrontal outflow obstruction were 9% by obliteration and 9% by cranialization.32

Temporal Bone Skull Base Fractures


Clinical signs of trauma to the middle cranial skull base include hemotympanum, otorrhea, postauricular hemorrhage (Battle sign), facial palsy, vertigo, and tinnitus. Temporal bone fractures are classified relative to the long axis of the petrous pyramid. Longitudinal temporal bone fractures, comprising 70% to 90% of temporal bone fractures, result from direct trauma to the lateral temporoparietal skull and run lengthwise through the petrous bone (Fig. 136-4).7173 Conductive hearing loss due to disruption of the ossicles is more common with longitudinal as compared to transverse temporal bone fractures. Facial nerve injury occurs in approximately 10% to 25% of longitudinal fractures. The site of facial nerve injury in longitudinal fractures most often localizes to the region of the geniculate ganglion.74

By contrast, transverse temporal bone fractures comprise 10% to 30% of temporal bone fractures and occur perpendicular to the petrous axis (Fig. 136-5). They arise as a result of significant trauma to the occipital skull. A typical fracture begins in the suboccipital bone at the site of impact and extends toward the foramen magnum coursing forward at right angles through the petrous temporal bone, often to the foramen lacerum. Damage to the labyrinth, cochlea, or cranial nerve VIII commonly leads to sensorineural hearing loss. Immediate facial nerve paralysis occurs in 30% to 50% of transverse temporal fractures. The facial nerve is typically injured in the proximal region of the labyrinthine segment or internal meatus.74 Extension of a transverse fracture to the jugular foramen may also cause lower cranial nerve dysfunction.


Fractures of the temporal bone may be exposed by two main approaches: an extradural, subtemporal exposure and a transmastoid approach. The specifics of the fracture, site of facial nerve injury, or both determine the approach. For longitudinal fractures, a middle fossa subtemporal approach is generally used. The patient’s head is positioned parallel to the floor, and a temporal craniotomy is performed through an incision anterior to the ear, above the zygoma. Dura is elevated from the floor of the middle cranial fossa, and the greater petrosal nerve and arcuate eminence are identified. The greater petrosal nerve is followed posteriorly to the geniculate ganglion and the site of facial nerve injury. If necessary, the tegmen tympani and internal auditory canal are opened, enabling exposure and decompression of the meatal, labyrinthine, and proximal tympanic segments of cranial nerve VII.75

For transverse temporal bone fractures, a transmastoid approach is generally indicated if hearing is preserved. A transmastoid approach through a retroauricular incision enables decompression of the facial nerve along its distal tympanic and mastoid segments.75,76 If serviceable hearing is absent, the labyrinthine and geniculate courses of cranial nerve VII can be decompressed through a translabyrinthine approach. Some believe, however, that even trace cochlear function justifies a labyrinthine-sparing approach.75 The nerve is decompressed or repaired by a primary or interposition anastomosis. Fat and fibrin glue are used to fill the mastoidectomy cavity. If a proximal segment of normal facial nerve is not identified, the mastoid exposure can be extended to open the posterior fossa and a proximal stump of the facial nerve can be identified at the brain stem and sutured to an interposition sural nerve graft.77

Suboccipital Skull Base Fractures

In contrast to anterior fossa floor and petrous temporal skull base fractures, wherein the site of impact may be remote from the fracture site, fractures of the suboccipital bone generally arise at the site of direct impact. Falls backward from standing and assaults are the most common mechanisms of injury. Displaced and nondisplaced fractures of the suboccipital bone may be associated with injury to the underlying major venous sinuses. Trauma of force sufficient to fracture the suboccipital bone and skull base should flag a careful assessment of cranial–cervical stability.76,78 Occipital–cervical dislocation injuries are usually fatal (Fig. 136-6).7880 Suboccipital fractures should also heighten awareness for possible vertebral artery injury.

Fractures of the suboccipital bone may extend to involve the occipital condyles. Occipital condyle fractures are classified into three types.81 They are associated with cranial nerve deficits in upward of one third of cases.82 Dynamic flexion–extension views and magnetic resonance imaging are useful adjuncts to evaluating the stability of occipital–condyle fractures.83 Most are stable and can be managed in a cervical orthosis without need for operative intervention.84,85

Decompressions for Skull Base Trauma

Decompressive Hemicraniectomy for Supratentorial TBI with Associated Skull Base Injury


Skull base trauma entails transmission of large forces to the cranium, and not surprisingly these patients frequently require surgery for supratentorial injuries. Decompressive hemicraniectomy is a surgical procedure in which a large area (about 12 × 15 cm) of skull bone is removed to treat brain swelling and raised ICP.8689 An emergent or primary decompressive craniectomy is performed when the initial CT scan in the emergency department shows a mass lesion with indications for operative intervention. At the time of surgical evacuation, the bone is not replaced to accommodate anticipated postoperative brain swelling. By comparison, a delayed decompressive craniectomy is performed to relieve raised ICP that has become refractory to medical management in the ICU.


The techniques of a decompressive craniectomy have been reviewed elsewhere.90 Additional considerations and risks accompany a decompressive craniectomy performed in the setting of associated skull base trauma. Upon elevation of the craniectomy bone flap, inaccessible and uncontrolled bleeding may be evident from the depths of a skull base fracture. This is especially common in the area of the sphenoid wing and the middle cranial fossa floor. The source of the bleeding may be the fracture, or it may signify the presence of a vascular injury within the skull base, such as an injured carotid artery (Fig. 136-7) or middle meningeal artery (Fig. 136-8). The presence of a hematoma along the floor of the middle cranial fossa on CT scan should alert the surgeon to the possibility of active bleeding from the skull base (Fig. 136-8

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