Craniofacial and skull base trauma.Katzen JT, Jarrahy R, Eby JB, Mathiasen RA, Margulies DR, Shahinian HK.

Source

Department of Surgery, Division of Trauma Surgery, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.

Abstract

BACKGROUND: Traumatic craniofacial and skull base injuries require a multidisciplinary team approach. Trauma physicians must evaluate carefully, triage properly, and maintain a high index of suspicion to improve survival and enhance functional recovery. Frequently, craniofacial and skull base injuries are overlooked while treating more life-threatening injuries. Unnoticed complex craniofacial and skull base fractures, cerebrospinal fluid fistulae, and cranial nerve injuries can result in blindness, diplopia, deafness, facial paralysis, or meningitis. Early recognition of specific craniofacial and skull base injury patterns can lead to identification of associated injuries and allow for more rapid and appropriate management. CONCLUSION: Early detection and treatment of craniofacial and skull base traumatic injuries should lead to decreased morbidity and mortality. This review discusses the most common of these injuries, their possible complications, and treatment.

Craniofacial and Skull Base TraumaBy J. Timothy Katzen M.D., Reza Jarrahy M.D., Joseph B. Eby M.D., Ronald A. Mathiasen M.D., Daniel R. Margulies M.D., FACS, Hrayr K. Shahinian M.D, FACS

Abstract: Background

Traumatic craniofacial and skull base injuries require a multidisciplinary team approach. Trauma physicians must evaluate carefully, triage properly, and maintain a high index of suspicion to improve survival and enhance functional recovery. Frequently, craniofacial and skull base injuries are overlooked while treating more life-threatening injuries. Unnoticed complex craniofacial and skull base fractures, cerebrospinal fluid fistulae, and cranial nerve injuries can result in blindness, diplopia, deafness, facial paralysis, or meningitis. Early recognition of specific craniofacial and skull base injury patterns can lead to identification of associated injuries and allow for more rapid and appropriate management.

Abstract: Conclusion

Early detection and treatment of craniofacial and skull base traumatic injuries should lead to decreased morbidity and mortality. This review discusses the most common of these injuries their possible complications and treatment.

Keywordscraniofacial trauma, skull base trauma, facial fractures, temporal bone fractures, anosmia, diplopia, otorrhea, rhinorrhea, CSF leaks, cranial nerve trauma, mandible fractures, maxillary fractures, LeFort fractures, zygomatic fractures, orbital fractures

Introduction

In the United States in 1999, there were over six million automobile crashes. Over two million crashes resulted in injuries with over thirty-seven thousand deaths.1 Over 75% of these injuries have craniofacial or cervical spine injury.2 With the advent of ever increasing sophistication in computed tomography (CT) imaging, trauma surgeons can diagnose rapidly small facial fractures and intracranial hemorrhages. However, despite imaging

improvements and more thorough physical examination, subtle complex facial fractures with cerebrospinal fluid (CSF) leaks, temporal bone fractures, and cranial nerve injuries can remain undiagnosed. Unfortunately, delayed or missed diagnoses can lead to significant morbidity (blindness, diplopia, deafness, facial paralysis, and meningitis) or death. Greater awareness of potential cranial injuries is needed to facilitate more rapid diagnosis and appropriate treatment.

A careful history and physical examination is paramount to accurately diagnose craniofacial injury. After performing the primary survey outlined by advanced trauma life support, a more thorough secondary survey should proceed systematically. The clinical examination of the craniofacial skeleton begins with inspection for localized tenderness, numbness, bleeding, asymmetry, deformity, ecchymosis, periorbital edema, otorrhea, and rhinorrhea. All bony surfaces should be palpated including the superior and inferior orbital rims, zygomatic arches, nose, maxilla, mandible, and both alveolar ridges. Even if the eye is swollen shut, both eyes should be examined closely; examination should include visual acuity and extraocular muscles. Midface stability should be appraised. Alveolar ridges and teeth should be examined for dental trauma and occlusion should be assessed.3, 4

In the conscious and cooperative patient, a detailed cranial nerve (CN) examination should be performed. The optic nerve, CN II, is assessed by visual field acuity. Extraocular movements test the integrity of CN III, IV, and VI.5 Hypoesthesia of the face suggests CN V injury. Facial nerve injury, CN VII, produces paresis or paralysis of the muscles of facial expression.

The cranial nerve examination of the comatose patient is slightly more difficult and relies on testing of brain stem reflexes.6 In the comatose patient, assessing vision can be difficult; even with complete unilateral visual loss, pupils can remain equally reactive as long as the efferent pathway of CN III is intact.7 The optic and oculomotor systems should be evaluated by the "swinging flashlight test". The test requires an intact afferent CN II pathway and an intact efferent CN III parasympathetic pathway.7 Testing patients with unilateral afferent CN II damage reveals bilateral, equal pupillary constriction when light is directed toward the eye with vision. However, when light is directed toward the eye with diminished vision, bilateral pupils will dilate. The phenomenon is referred to as the Marcus Gunn pupil.7 In the comatose patient, extraocular movements can be tested with the oculocephalic (or "doll's eye") reflex. The corneal reflex consists of touching the cornea with a piece of cotton; afferent fibers of CN V send the message to the brain and CN VII responds by eyelid closure. CN VIII is assessed with the cold-water caloric test, in which ice water is injected into the ear and elicits nystagmus. Testing of the gag reflex evaluates CN IX and CN X.

After careful physical examination, the trauma surgeon should focus on specific areas of common craniofacial injuries.

Craniofacial fractures

Orbital fracturesForceful impact to the skull can cause a fracture along the weak points of the orbit. The thinnest and weakest area of the orbit is the floor. Typically, the posteromedial region of the orbital floor is fractured. Often, orbital soft tissues herniate inferiorly into the maxillary sinus and become entrapped.8 Entrapment of the inferior oblique or inferior rectus muscle can lead to diplopia and restriction of globe movement. Additionally, the globe is displaced posteriorly and inferiorly, which causes enophthalmos and further diplopia.

The degree of orbital floor displacement is diagnosed accurately with axial and especially, coronal CT scans of the orbit and facial bones. Surgical intervention is indicated when there is significant orbital floor disruption, persistent diplopia, entrapment, or enophthalmos.9 Surgical access to orbital floor fractures involves a subciliary or transconjunctival incision in the lower eyelid. 9 The incarcerated orbital tissue is reduced and bony defects are reconstructed with a variety of allografts or autografts harvested from assorted sites.

Fractures of the superior, lateral, and inferior orbital rims may occur in isolation or in conjunction with other

craniofacial fractures. Physical examination may reveal step-offs in the line of the fracture. Cheek paresthesias are common due to inferior orbital rim fractures traumatizing the infraorbital nerve.

Orbital fractures are repaired by realignment and fixation with miniplates. 10

Zygomatic fracturesThe zygoma forms the malar eminence, determines anterior and lateral cheek projection, and supports the lateral orbital wall and floor. The zygoma has four processes. Superiorly, the frontal process articulates with the frontal bone at the zygomaticofrontal suture. Inferiorly, the maxillary process articulates with the maxilla at the zygomaticomaxillary suture. Laterally, the temporal process joins the temporal bone, anterior to the external auditory canal. Medially, the orbital process articulates with the greater wing of the sphenoid.

Due to the projection of the zygoma, traumatic injury is common. Most zygomatic fractures occur in the arch and include a portion of the lateral orbital wall.11, 12 Zygomatic arch fractures cause depression of the cheek due to the pull of the masseteric muscle in an inferior, medial, and posterior vector. 12 Subconjunctival hematomas and infraorbital nerve paresthesias are so common, that their absence makes the diagnosis of zygomatic fracture questionable.13

Many zygomatic fractures are minimally displaced and do not require surgical correction. Non-comminuted, posterior zygomatic arch fractures can be treated through a 1 cm temporal incision by simple reduction, without the need for internal fixation.12 However, any other displaced zygomatic fracture requires open reduction and internal fixation.13 Successful reduction relies on an accurate three-dimensional reduction with an emphasis on careful realignment of the lateral orbital wall.14 Fractures are reduced and secured with miniplates.

Maxillary fracturesMaxillary fractures result from direct blows. Transmitted forces follow a predictable path along the thinner portions of the maxilla. The predictable patterns form the basis of the LeFort classification of maxillary fractures.15 LeFort I fractures are the most caudal of maxillary fractures. LeFort I begin in the lower margin of the piriform aperture and extend laterally above the roots of the teeth, through the anterior maxillary wall, and posterior-laterally to involve the pterygoid processes. LeFort II fractures are centrally more cephalad and due to their shape, are called "pyramidal fractures". LeFort II fractures begin at the nasal bridge, extend inferior-laterally inside the medial orbit, exit through the infraorbital foramen, travel through the zygomaticomaxillary suture, and extend posteriorly to involve the pterygoid processes. LeFort III fractures begin medially as LeFort II fractures; however, instead of exiting the orbit over the infraorbital rim, they progress laterally along the entire orbital floor and extend to disrupt the zygomaticofrontal suture. LeFort III fractures result in complete craniofacial dysjunction because the facial bones and structures of the middle third of the face become totally separated from the cranium.

The original facial fracture studies done by Dr. Rene LeFort were performed on cadavers sustaining direct blows to the center on the face.16 Since most facial trauma consists of blows from the side or slightly off center, ideal, symmetric LeFort I, II, and III patterns are rarely followed.14 Most maxillary fractures are more comminuted on one side than the other. Thus, LeFort fractures may be seen in any combination: a right "hemi" LeFort II fracture can coexist with a left "hemi" LeFort III fracture.14

Prolonged delay in the operative repair of maxillary fractures results in poor healing and should be discouraged.12 One of the major goals in the treatment of LeFort fractures should be reestablishment of pre-injury dental occlusion. Therefore, LeFort fracture patients should always be placed in intermaxillary fixation, prior to open reduction and internal fixation. A second, but equally important goal in the treatment of LeFort fractures should be reconstruction of the orbital floor (see Orbital fractures above). A third goal should be reestablishment of the patient's facial height and projection; pre-traumatic facial form can be achieved by accurate open reduction and internal fixation.

Mandibular fractures

Along with the zygoma, the mandible is one of the most frequently fractured facial bones and constitutes approximately 20% of all facial fractures.18 Areas of mandibular weakness are the most likely to fracture and include the mandibular neck, subcondylar region, and angle.18 Since greater than 50% of mandibular fracture in two or more locations, a second fracture site most always be suspected when examining a patient.18

Presence of teeth, position of mandibular fracture, and pull of mandibular musculature all determine presenting symptomatology. Mandibular fractures frequently present with malocclusion and asymmetry.18 The most important goal in the treatment of mandibular fractures is to reestablish the patient's pre-injury dental occlusion.18 Most mandibular fractures require open reduction and internal fixation. Due to the bacterial load of the mouth, open mandibular fractures should be irrigated immediately, reduced and fixated. Closed mandibular fractures should be openly reduced and internally fixated within three to five days after the injury, to allow for deceased edema and intra-operative bleeding. If there is any question as to the stability of a mandibular fracture, the patient should be left in intermaxillary fixation for four to six weeks to ensure proper bone healing.18

Skull base fracturesFive bones form the base of the skull. The bones include the orbital plate of the frontal bone, cribriform plate of the ethmoid bone, sphenoid bone, occipital bone, and the squamous and petrous portions of the temporal bone. Up to 24% of patients sustaining blunt head trauma have a skull base fracture.20 Despite the clinical importance of skull base fractures, many are undiagnosed. Because of the complex anatomic relationships of the skull base, the fractures may damage critical neighboring structures, including cranial nerves, internal carotid artery, and cavernous sinus. The fractures may lacerate the dura and create a potential CSF fistula.

When a fracture of the skull base is suspected, insertion of a nasogastric tube (NGT) should be avoided. The orogastric route is preferred as there have been cases of intracranial NGT placement in the presence of cribriform plate fractures.21

Temporal bone fractures

Clinical signs of temporal bone fractures include blood in the external auditory canal, hemotympanum, ecchymosis overlying the mastoid bone, otorrhea, hearing loss, vestibular dysfunction, and facial nerve paresis or paralysis. High-resolution non-contract CT scan should be performed in all suspected temporal bone injuries.22 Coronal sections and 3D reconstructions provide information about the facial nerve canal, carotid canal, and otic capsule.

Temporal bone fractures are classified according to their relationship to the long axis of the petrous pyramid. Though most temporal bone fractures are mixed, temporal bone fractures are classified as longitudinal or transverse.

Seventy to ninety percent of temporal bone fractures are longitudinal, and occur after direct lateral blows to the temporoparietal skull.22, 23 These fractures usually begin in the weaker squamous portion of the temporal bone and course toward the carotid and jugular foramina. Usually, the tympanic membrane is torn and the middle ear ossicles are disrupted resulting in a conductive hearing loss. Bleeding from the external auditory canal is common. Approximately 25% of patients have facial nerve injury, which usually occurs in the geniculate ganglion or facial canal.

Transverse temporal bone fractures are much more rare and occur following severe trauma to the occiput.24 These fractures begin in the jugular foramen and course across the petrous pyramid, through the foramina spinosum and lacerum to the foramen magnum. Approximately 50% of patients notice immediate facial paralysis from CNVII injury.25 Unless corrected surgically, facial paralysis may be permanent. Typically, CNVII is injured in the internal auditory meatus or on the medial wall of the tympanic membrane. In addition, damage to the labyrinth, cochlea, or CNVIII can result in sensorineural hearing loss and vestibular dysfunction.

Transverse temporal bone fractures often course through the otic capsule. Because the otic capsule heals by fibrous union rather than bony callus formation, patients have a lifelong risk for developing meningitis.26

Penetrating temporal bone traumaPenetrating trauma to the temporal bone usually results from self-inflicted gun shot wounds.27 After initial stabilization, a complete vascular and neurologic evaluation should be performed. Vascular examination should include digital subtraction angiography with venous phasing or magnetic resonance angiography.28 Complete neurologic examination should place special emphasis on cranial nerves examination. Due to the close proximity of vital structures, one neurologic deficit may point towards another injury. For example, vocal cord paralysis from an injured vagus nerve may be associated with a carotid artery or jugular vein injury.

Skull base fracture treatment

In the absence of a CSF fistula, temporal bone fracture, facial paralysis, hearing loss, or blindness, the management of skull base fractures is nonoperative and expectant. Conservative treatment includes a five days course of intravenous antibiotics to allow potential dural tears to heal.20

Operative treatment is indicated for post-traumatic CSF fistulae with meningitis, transverse petrous fractures with otic capsule involvement, temporal bone fractures with complete facial paralysis, and ballistic injury to the temporal bone.29 Treatment includes a subtotal petrosectomy. The operation consists of complete exenteration of temporal bone air cell tracts and obliteration of the eustachian tube.26 After the injured structures are repaired (e.g., the facial nerve or carotid artery) or exenterated (e.g., the otic capsule), the resulting cavity is obliterated with an endogenous fat graft and temporalis muscle flap

CSF FistulaeApproximately 20% of skull base fractures will develop a CSF fistula with 80% occurring within 48 hours of injury.30, 31 Manifestations include rhinorrhea and otorrhea. The drainage is usually clear and nonmucoid and may be difficult to detect when mixed with blood. To facilitate the diagnosis of CSF leak, a few drops of the fluid are placed on a tissue paper. CSF has a more rapid diffusion pattern than blood, and when the discharge is mixed with blood, a larger, clearer CSF ring will surround the sanguineous central ring. The clinical finding is termed the "double-ring" sign. Alternatively, the fluid glucose concentration can be measured. Values should be compared to serum glucose levels and quantities greater than 30 mg/dl are usually consistent with CSF.32 In addition, the fluid should be sent for beta-2-transferrin. Presence of beta-2-transferrin confirms a CSF leak.

RhinorrheaCSF draining from the nose results from fractures through the cribriform plate, ethmoid, sphenoid, petrous portion of the temporal bone, or orbital plate of the frontal bone.33 Initially, patients are managed conservatively. Patients are maintained at total bed rest with the head of bed elevated, to reduce the flow of CSF drainage. If drainage has not ceased after 72 hours of conservative therapy, a lumbar drain should be inserted to drain 150ml of CSF per day for three to four days. Diversion of CSF from the site of the dural tear facilitates spontaneous closure. Current data support placing patients on 1 to 2 million units of penicillin per day in the presence of a CSF fistula.34, 35 Nasal and throat cultures should be taken, and antibiotics should be selected upon culture results.

The CSF fistula is localized with CT scans using 3.0 mm coronal sections. Two other studies may help localize the fistula: an indium-111 DTPA or metrizamide CT cisternogram. An Indium-111 cisternogram begins with the placement of cotton pledgets in the anterior and posterior roof of the nose, sphenoethmoidal recess, and middle meatus.36 Indium-111 DTPA is introduced into the spinal subarachnoid space via lumbar puncture. The patient's head is flexed, causing an increase in intracranial pressure and thereby increasing the flow of CSF through the dural tear. The radioactivity of the cotton pledgets is measured and used as a guide to the site of the leak. A metrizamide CT cisternogram begins by introducing metrizamide into the lumbar subarachnoid space. Then the patient undergoes a coronal CT scan. Contrast material will be seen in the paranasal sinuses near the fistulous tract. An actively draining fistula is required for the technique. Since most fistulae drain only

intermittently, false-negative studies are common.

After localizing the site of the CSF fistula, operative repair may be undertaken. However, there is no consensus regarding the timing of operative repair. Current recommendations for patients with an isolated CSF fistula include deferring surgery for at least five days.20, 31, 37 Surgical intervention should be reserved for patients with meningitis, large defects with brain herniation into paranasal sinuses, pneumocephalus, or persistent CSF leak over five days.31, 37

Recent advances in endoscopy allow for a minimally invasive fully endoscopic transethmoidal or transsphenoidal approach to repair CSF fistulae.38 The technique is best utilized to access leaks through the sphenoid and ethmoid sinuses and the sella turcica.35

OtorrheaDrainage of CSF from the ear results when a fracture of the petrous portion of the temporal bone both tears the dura mater and perforates the tympanic membrane. CSF drainage can also occur from fractured mastoid air cells causing a laceration of the external auditory canal.

As with rhinorrhea, the initial management of otorrhea is conservative. The patient should be positioned to minimize fistula drainage. Irrigation and probing of the ear increase the risk of meningitis and should be discouraged. Most patients will stop draining spontaneously within several days. Rarely, otorrhea persists beyond five to seven days. When otorrhea lasts beyond seven days, high-resolution CT scanning with coronal sectioning should be performed to localize the site of the fracture. Detailed auditory and vestibular testing should be performed at six to eight weeks to diagnose abnormalities.

Operative intervention consists of a middle or posterior fossa craniotomy, fashioning a bone flap to expose the dura overlying the petrous bone.35 Primary repair is attempted, but if not possible, a graft of pericardium or fascia lata is used. Occasionally, endogenous fat or muscle is used to pack the defect.

Cranial nerve injuriesUpon exiting the skull, cranial nerves are especially prone to damage. Skull base fractures particularly predispose patients to cranial nerve damage. Table 1 lists the twelve cranial nerves and the common neurologic deficits following injury.

Olfactory nerve (CN I) injury

Injury to the olfactory nerve results in anosmia. Typically, anosmia occurs from anterior fossa floor fractures. In almost half of the cases, a patient's sense of smell returns in several months.39 In addition to a CT scan, work-up may require an olfactory electroencephalogram. Most of CNI injuries can be managed conservatively.

Optic nerve (CN II) injuryOptic nerve injury can result in blindness. Optic nerve injuries are usually due to isolated fractures of the optic canal or orbit or extensions of skull base fractures.40 Skull base fractures involving the sphenoid body and extending through the sella turcica and pars petrosa can damage the optic chiasm, producing blindness or bitemporal hemianopsia.41

The optic nerve is unique and not a true cranial nerve. The optic nerve is a direct extension of the brain and thus, the axons of the optic nerve do not regenerate. Therefore, prognosis is poor following optic nerve injury. With complete optic nerve transection distal to the optic chiasm, there is monocular blindness, a dilated pupil, and an absent pupillary reflex.42

Results of surgical decompression of the optic nerve in the optic canal are similar to rates of spontaneous recovery.43 Surgical decompression is reserved for cases of a narrowed optic canal, bony fragment in the optic canal, or deterioration of previously good vision following head trauma.42

When indicated, acute decompression is conducted through a bifrontal craniotomy. Additionally, optic chiasm decompression may be accomplished using an endoscopic transsphenoidal approach.

Oculomotor nerve (CN III) injuryInjury to CNIII is typically from a direct, frontal blow. Trauma stretches and contuses CNIII upon entry into the brain, at the posterior aspect of the cavernous sinus. Clinically, patients complain of diplopia resulting from impaired extraocular movements. Examination reveals an ipsilateral dilated pupil and an inability to move the eye medially, superiorly, or inferiorly.

Fractures through the superior orbital fissure cause damage to CN III, IV, VI, and the ophthalmic division of V.44 The clinical result is the superior orbital fissure syndrome. Patients may present with paralysis of the levator, superior rectus, inferior rectus, inferior oblique, superior oblique, and lateral oblique muscles and anesthesia of the brow, upper lid, and forehead. When superior orbital fissure syndrome symptoms are accompanied by blindness, the complex is called the orbital apex syndrome and indicates involvement of the optic foramen.

Treatment of ocular nerve palsies consists of wearing a patch over the affected eye. Spontaneous recovery of ocular movement usually occurs in four to six weeks.

Trochlear nerve (CN IV) injury

The trochlear nerve is the least frequently injured cranial nerve. Damage to cranial nerve IV results from stretching near the exit from the dorsal midbrain. Lateral rectus weakness results. Treatment is conservative and involves an eye patch to prevent diplopia. Function usually returns by four to six weeks.

Trigeminal nerve (CN V) injury

Injury to the trigeminal nerve causes sensory deficits to the face. The three branches of the trigeminal nerve are the supraorbital nerve (V1), the maxillary branch (V2), and the mandibular branch (V3).

V1 is damaged most commonly. The branch is particularly susceptible to injury at the supraorbital notch. Complete transection may result in anesthesia of the nose, eyebrow, and forehead.45 Typically, V2 is injured by maxillofacial fractures with resultant sensory defects of the ipsilateral cheek, upper lip, gums, and hard palate. Typically, V3 is injured by mandibular fractures and results in anesthesia of the chin.

Centrally, the trigeminal ganglion can be damaged by a penetrating head injury. This is associated with CN III, CN IV, or carotid-cavernous fistula.46 The nerve is especially vulnerable coursing through the dura, proximal to Meckel's cave.

Incomplete transection or scarring of the branches of CN V may result in intractable facial pain and neuroma formation. Corticosteroid injections, endoscopic decompression, or endoscopic division may be required for relief of symptoms.47

Abducens nerve (CN VI) injury

Injury to the CN VI results from fractures in the clivus. Vertical movement of the brainstem during trauma may stretch or avulse the nerve upon leaving the pons (Figure 9). As mentioned above, CN VI may be damaged in the superior orbital fissure and is classically accompanied by CN III and CN IV palsies.

The diagnosis of abducens palsy in the unconscious patient can be made when the affected eye fails to abduct as the head is passively turned away from the side of injury. Treatment is conservative and most cases of abducens nerve injury recover spontaneously after four weeks.

Facial nerve (CN VII) injuryTemporal bone fractures are the most common cause of facial nerve injuries.22, 25 Fifty percent of patients with transverse fractures of the temporal bone and 25% of patients with longitudinal fractures will have associated facial nerve injury causing ipsilateral facial paralysis.48

Although facial nerve injury within the temporal bone is the most common site, CN VII can be damaged anywhere along its course.49 In transverse temporal fractures, the nerve may be injured at the internal auditory meatus or in the horizontal portion of the fallopian canal. In longitudinal temporal fractures, the nerve may be damaged at the geniculate ganglion.

Following a detailed clinical examination, all patients suspected to have a facial nerve injury should have a CT scan and be evaluated with transcutaneous nerve excitability tests and electroneurography. Transcutaneous nerve excitability tests predict irreversible nerve injury by comparing the normal and injured side. When the difference is greater than 3.5mA, surgical intervention is usually required.50 Operative intervention is also indicated when there is complete, immediate, facial paralysis with greater than 90% denervation documented by electroneurography.51

Microsurgical techniques are utilized to explore, decompress, or directly repair the nerve. A subtotal petrosectomy approach is utilized. The severed nerve fascicles are sutured together under a microscope.

Most patients with traumatic facial paralysis recover well without surgical intervention; however, the eye must be guarded against exposure keratitis during the recovery period.25

Vestibulocochlear nerve (CN VIII) injuryDamage to the CN VIII is common following transverse fractures of the temporal bone from frontal or occipital impact. Cochlear and vestibular damage can result with deafness and labyrinthine dysfunction. In addition, fractures involving the otic capsule can lead to total degeneration of the cochlear and vestibular organs.

A baseline neuro-otologic evaluation should be done in all patients with head injury to detect hearing loss and vestibular dysfunction. Electronystagmography can be used to assess labyrinthine function. Auditometry and brainstem evoked potentials are used to evaluate hearing loss.

Previously, the prognosis of sensorineural hearing loss was poor. However, recent advances in cochlear implantation have allowed a return to speech understanding in 84% of patients following an intensive rehabilitation program.52

Glossopharyngeal (CN IX)Vagus (CN X)Spinal accessory (CN XI)Hypoglossal (CN XII) nerve injuryThe glossopharyngeal, vagus, and spinal accessory nerves exit the skull base in the jugular foramen. The hypoglossal nerve passes though the hypoglossal foramen just medial to the jugular foramen.

Injury to glossopharyngeal nerve produces dysphagia and loss of gag reflex. Vagus nerve injury results in paralysis of the ipsilateral vocal cord and resultant voice hoarseness. Spinal accessory nerve injury results in paralysis of the sternocleidomastoid muscle and weakness of the trapezius muscle; the result is weakness in contralateral head rotation and shoulder elevation. Hypoglossal nerve injury causes hemiatrophy of the tongue and ipsilateral tongue deviation. Treatment is usually supportive, employing physical, occupational, and speech therapy.

Conclusion

Because of the proximity of vital structures in the craniofacial and skull base region, localized trauma can result in unrecognized injuries. CSF fistulae and cranial nerve injuries in complex fractures can carry devastating consequences. Accordingly, appropriate surgical referral should be made whenever the injuries are suspected. Recent advances in skull base approaches have allowed for highly successful surgical correction of these potentially devastating injuries.

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Table 1. The 12 cranial nerves and the respective deficits following injury. Nerve Deficit (1) Olfactory Anosmia(2) Optic Blindness; Visual field deficits(3) Oculomotor Pupillary enlargement; Diplopia (paralysis of extraocular

muscles)(4) Trochlear Paralysis of superior oblique muscle causing diplopia(5) Trigeminal Loss of corneal reflex; Facial numbness; Weak muscles

of mastication(6) Abducens Inability to move the eye laterally causing diplopia on

lateral gaze(7) Facial Paralysis of muscles of facial expression(8) Vestibulocochlear Vestibular dysfunction; Nystagmus; Hearing loss(9) Glossopharyngeal Loss of gag reflex; Dysphagia(10) Vagus Vocal cord paralysis; Tachycardia(11) Spinal Accessory Paralysis of sternocleidomastoid(12) Hypoglossal Ipsilateral tongue deviation and atrophy

Skull base fractures

Introduction

Skull base fractures are of high importance in neurotrauma. They occur in 3.5 - 24% of head injuries and are often related to brain injury (in 50% of the cases).

70% of the skull base fractures occur in the anterior fossa, 20% in the middle central skull base and 5% in the middle and posterior fossa.

Traumatic (CSF) leakageThe most relevant clinical sign related to skull base fractures is CSF leakage. It occurs in 2% of all head trauma and can reach 30% of all skull base fracture cases.

80% of the traumatic CSF leakage occurs within 48 hours after injury.

16% of cases are “occult“, being found after recurrent meningitis.

Anatomy

IntroductionWe consider the endocranial (inner) surface of the skull base, which consists of the cranial cavity on which the brain rests, and  the exocranial (external) surface. The bones which form the skull base are:

Frontal bone Sphenoid bone Temporal bone Occipital bone

The anterior part of the exocranial surface is also formed by the:

Zygomatic bone Maxillary bone Palatine bones

The bones of the skull base contain several foramina through which nerves, arteries, and veins pass.

Anatomically, the inner surface of the skull base is formed by:

Anterior fossa Middle fossa Posterior fossa

Anterior fossaThe anterior fossa is formed by the ethmoid bone, sphenoid bone and frontal bone. It is limited anteriorly by the frontal bone and the posterior wall of the frontal sinus, posteriorly by the limen of the lesser wing of the sphenoid bone. The lateral parts form the roof of the orbits. The median (central) part is formed by the crista galli, the cribriform plate of the ethmoid plane and the planum of the sphenoid bone.

Middle fossaThe middle fossa is formed by the sphenoid and temporal bones. It is limited anteriorly by the lesser wings of the sphenoid bones, posteriorly by the petrous bones.

Posterior fossaThe posterior fossa is formed by the occipital bones. It is limited anteriorly by the posterior walls of the petrous bones and posteriorly by the grooves of the transverse sinuses.

Extension of anatomical classificationBy drawing two horizontal lines which reach the lateral margins of the optic canals, the skull base can be divided into three longitudinal regions:

Central skull base Lateral skull base (left and right)

Thereby, the inner surface of the skull base is divided into 9 quadrants.

Central skull baseThe anterior central skull base (a CSB) covers the upper nasal cavity and the sphenoid sinus.The middle central skull base (m CSB) contains laterally the cavernous sinuses with the carotid arteries inside (parasellar compartments).The posterior central skull base (p CSB) includes the clivus reaching the anterior margin of the great occipital foramen.

Cranial nerves and related skull base foraminaWhen fractures involve some specific anatomical regions the involvement of nerves passing through a foramen in the respective region should be always considered.

I Olfactory nerve: formed by many sensory nerve fibers that extend from the olfactory epithelium to the olfactory bulbs passing through the openings of the cribriform plates of the ethmoid bone (in the anterior central skull base).

II Optic nerve: passes from the retina to the brain in the optic canal in close relationship with the anterior clinoid process (middle central skull base).

III Oculomotor nerve: enters the orbit through the superior orbital fissure between the middle and anterior fossae.

IV Trochlear nerve: enters the orbit through the superior orbital fissure between the middle and anterior fossae.

V Trigeminal nerve: is made up of three divisions:

Ophthalmic branch which passes through the superior orbital fissure Maxillary branch which passes through the foramen rotundum

Mandibular branch which passes through the foramen ovale

VI Abducens nerve: enters the orbit through the superior orbital fissure between the middle and anterior fossae.

VII Facial nerve: enters the petrous temporal bone via the internal auditory meatus and emerges from  the external surface of the skull base through the stylomastoid foramen (lateral posterior skull base)

VIII Vestibulocochlear nerve: enters the internal acoustic meatus.

IX Glossopharyngeal nerve: passes the through the jugular foramen.

X Vagus nerve: passes the through the jugular foramen.

XI Accessory nerve: starts outside the skull, enters the skull through the foramen magnum and exits again with the IX and X nerve through the jugular foramen.

XII Hypoglossal nerve: passes through the hypoglossal canal in the occipital bone.

Extracranial surfaceThe extracranial surface is formed by:

Occipital bones Temporal bones Sphenoid bones Palatine bones Zygomatic bones

The specific structures that can be involved in fractures of the extracranial surface of the skull base are the:

Styloid processes of the temporal bone

Tips of the mastoid bones Occipital condylar processes

Mechanism of the injury

The skull base is particularly susceptible to the effects of blunt trauma. Skull base fractures are often associated with cranial vault or midface fractures.The most vulnerable regions of the skull base are the petrous bone, the sphenoid sinus, and the foramen magnum.

Clinical presentation

Since skull base fractures are the results of high force impacts and are often associated with other intracranial injuries. Therefore, patients may be unconscious or require intervention for other more life-threatening injuries. As a result, the clinical signs and symptoms of skull base fractures may not be recognized immediately.

Patients affected by skull base fractures can present anywhere from awake and asymptomatic to comatose or even moribund.

The first clinical assessment is the evaluation of the Glasgow coma scale (GCS).

It is important to recognize the blood and/or CSF coming from the ear (otorrhea), the nose (rhinorrhea), or some calvarial wounds. CSF leakage must be identified since it poses high risk for meningitis. For suspected but not evident rhinorrhea a provocation test (Valsalva maneuver) can be useful. Other useful test can be:

Double ring sign Glucose test strip Beta-2-transferrin test

The presence of subcutaneous ecchymosis in the mastoid region (Battles’ sign) or ...

... around the eyes (raccoon’s eyes) is very highly suspicious for skull base fractures.

In awake patients it is important to identify the presence of cranial nerve injury as soon as possible especially of the optic and facial nerves.

A complete neurological examination has to be done in all cases. 

Imaging

The gold standard for the radiographic detection of skull base fractures is computed tomography.

Specific, very useful CT sequences are:

Non contrast high resolution bone window CCT (thin slices 1mm, axial and coronal) Multiplanar reconstructions

Special modalities include:

MRI Cerebral angiography CT-cisternography

Classification

Single (linear and/or branched) and multipleThe fractures can be single, crossing more bones, or multiple, in the same bone or in different bones. The fracture can be linear or branched.

Single fracture line

Branched fracture lines.

Multiple separated fracture lines.

ComminutedA fracture is comminuted when the bone is shattered into many fragments.

Contiguous The fracture is contiguous when it crosses anatomical boundaries.

Depressed The fractured segments are displaced inward, toward the meninges and brain for more than 3 mm.

Diastatic sutureHorizontal displacement along the cranial sutures (>3 mm).

Diastatic fractureHorizontal displacement of the bones at the margin of the fracture (>3 mm).

Cranial Vault & Skull Base Authors

Overview

Lacerations

Soft-tissue injuries can be used to directly access fracture sites for fracture management.

Coronal approach

The coronal or bi-temporal approach is used to expose the anterior cranial vault, the forehead, and the upper and middle regions of the facial skeleton.

Lateral skull base approach

With the lateral skull base approach the lateral anterior and the middle cranial fossae can be reached.

Posterior skull base approach

When wide visualization of the medial canthal area, lacrimal sac, and medial orbital wall is needed an extended glabellar approach is advantageous.

Transmastoid approach

The transmastoid approach is used for facial nerve decompression. A postauricular incision is commonly used to access the mastoid.

Endoscopy: Transnasal

Endoscopic sinus surgery techniques can be used to open the frontal recess from below.

Endoscopy: Central skull base

The whole central compartment of the skull base, from the crista galli to the clivus and anterior craniocervical junction, can be accessed by means of the endonasal transsphenoidal endoscopic approach.

Endoscopy: Anterior table

Endoscopy has a variety of potential uses for frontal sinus fractures. Endoscopic access is most favorable in the upper portion of the frontal sinus.

Endoscopic repair of CSF leak

1.   Introduction

Traumatic CSF rhinorrhea occurring in the anterior and/or middle cranial fossa can be treated by endoscopic techniques associated with lumbar intrathecal administration of fluorescein.

The illustration shows the region that can be reached endoscopically.

2.   Tools required

Tool required for the endonasal endoscopic repair are:

Endoscopic set (0°, 30°, and 45° endoscopes) Fluorescein blue-light filter system coupled to the light source Fluorescein

3.   Sequence of procedure

The steps for the surgical procedure are:

Lumbar intrathecal fluorescein injection Endonasal endoscopy and identification of the defect Repair of the defect

4.   Fluorescein injection

In the majority of cases before surgery a lumbar drainage is inserted which allows the injection of 1 ml sodium fluorescein (0.5%). Using a lumbar drainage offers the advantage to re-inject fluorescein during the surgical procedure if needed.

5.   Endonasal endoscopy and identification of the defect

The patient can be positioned supine on the operating table with the trunk raised between -10° up to +45°. The head can be rotated toward the surgeon if necessary. The endoscope is inserted in the nostril (right, left, or both) and the anatomical landmarks are visualized. The use of navigational devices (fusion data sets, CT, and MRI) is helpful.

6.   Identification of the anatomical landmarks

For the endoscopic anatomical orientation the following structures should be identified:

Nasal septum (NS) Middle turbinate (MT) Choana (C) Sphenoid ostium (OS)

7.   Methods of approach

Endonasal endoscopy can be performed by several methods depending on the type of lesion and its location. The classic approach to the olfactory fossa is the direct paraseptal one (with or without removing any ethmoidal structures according to the anatomical variations of the patient).

8.   Identification of the lesion

The use of a fluorescein blue-light filter system and the fluorescein barrier filter mounted to the eyepiece of the endoscope might be helpful to visualize the localization of the dural defect. A CSF fistula, if present, is seen with a characteristic green glow.

Click here to see video demonstrating this.

9.   Repair of the defect

Several techniques exist for the repair of the defect and different grafts can be used including autologous nasal, extra-nasal, and heterologous grafts. The bone defects can be repaired using septal cartilages, parts from the middle nasal turbinates, eventually the vomer, etc. The most used autologous extranasal graft is the abdominal fat or the fascia lata. In larger defects, a vascularized nasoseptal flap can be used.

The closure technique is a strictly related to the individual patient‘s anatomy, the size of the leak, and its anatomical location. Underlay, overlay, combined, and obliterative techniques have been described. The illustration shows a combined three layer technique in which are evident:

Subdural intracranial underlay graft (dark green) Extradural intracranial underlay graft (blue) Extracranial overlay graft (purple)

Fibrin glue can be used to keep the layers together or to fill the dead-space.

10.   Confirmation of proper closure

After closing the defect, its efficacy and reliability is checked using a Valsalva maneuver and in special cases, intraoperative fluorescein test.

Appendix

Late sequelae

1.   Introduction Complications and late sequela of cranial vault/anterior skull base fractures typically include: Mucocele/Mucopyocele of the frontal sinus Osteomyelitis Contour deformities Infection of (allogeneic) grafts Late CSF leak Meningitis

These sequela may occur even decades after the initial injury and often require surgical management.

The risk for late sequela can be minimized by meticulously ensuring adequate drainage if the frontal sinus is preserved or meticulous removal of mucosa if it is obliterated. Patients with frontal sinus/anterior skull base fractures should be followed up for years.

Mucocele/Pyocele

Mucocele/pyocele is the most frequent late sequela after frontal sinus fractures and may occur many years after the accident. These complications are the result of mucosal proliferation after incomplete removal of the mucosa or inadequate drainage. Typical symptoms include pain, swelling, and globe displacement. Treatment with antibiotics may temporarily relieve the symptoms. However, due to the potentially serious complications (eg, meningitis, visual dysfunction) operative treatment should not be delayed for a long time.

If the mucocele is accessible and limited a transnasal endoscopic approach may be employed. Otherwise an open procedure should be performed.

2.   Operative techniques: Open approach

Indications and limitations

The open approach is indicated whenever the pathology involves regions of the frontal sinus which can not be addressed transnasally or if reconstruction of sinus walls or frontal bone is necessary. The coronal approach allows wide exposure of the sinus and naso-orbital-ethmoidal region and it allows for craniotomy if necessary. In addition, harvesting of cranial bone grafts can be done without an additional incision.

Technique Coronal approach Exposure of the frontal sinus Osteotomy of anterior table of frontal sinus Removal of infected material Meticulous removal of mucosa Reconstruction or obliteration of the frontal sinus: The technique of reconstruction may considerably

change depending on the specific problem. This is illustrated by the following collection of cases.

3.   Case example: Mucocele with globe displacement

Large mucocele of the left frontal sinus causing …

… caudal/lateral displacement of the globe.

Postoperative scan showing the osteotomy used for access and repair of the mucocele. The defect in the orbital roof was reconstructed with a cranial bone graft (arrow). Even though this mucocele could have been approached endonasally, reconstruction of the orbital roof would not have been possible.

4.   Case example: Partial obliteration of the frontal sinus

Mucocele affecting only the lateral two thirds of the right frontal sinus in a patient with previous titanium mesh reconstruction of the anterior table of the frontal sinus and recurrent infections. The drainage of the medial one third and of the left frontal sinus is intact.

Mucocele has resorbed the orbital roof causing recurrent orbital cellulitis.

Initial repair of the frontal sinus fracture had been achieved with a titanium mesh, reconstructing the anterior table defect.

After removal of the mesh, the frontal sinus can be inspected.

Reconstruction of the anterior table defect with bone.

In this case, only partial obliteration of the frontal sinus was done with fat and fascia, while the defect in the orbital roof and in the anterior table was reconstructed with cranial bone.

Considering the large communication between the frontal sinus and the ethmoidal sinus, partial obliteration was considered to be technically less difficult.

5.   Case example: Infection of a hydroxyapatite graft

Chronic infection with recurrent fistulae 5 years after obliteration of the frontal sinus with hydroxyapatite cement. The use of hydroxyapatite cement in direct communication with the nasal cavity is not recommended due to the high complication rate.

Exposure of the cement to the nasal cavity resulted in contamination and infection of the alloplastic graft.

If hydroxyapatite is chosen for obliteration of the frontal sinus, contact to the nasal cavity must be avoided.

Dissolution of the graft by granulation tissue.

After removal of the graft the nasal root (see arrow) is mobile.

Stabilization of the nasal root and reconstruction of the supraorbital rim with cranial bone.

Communication to the nasal cavity is sealed with fascia (arrow).

The frontal sinus cavity is obliterated with fat and the anterior table is reconstructed with titanium mesh.

6.   Case example: Infection of a PMMA graft causing recurrent fistulae

Patient 20 years after extended frontal sinus fracture. In the initial repair, obliteration of defects was achieved with PMMA. Ten years after the accident, recurrent fistulization occurred. Repeated local excisions were unsuccessful.

MRI shows a defect in frontal bone communicating with the fistula.

Intraoperative view showing the PMMA graft embedded into granulation tissue.

After debridement the contour of the bone is restored with a titanium mesh and the defect is filled with fat.

The fistula is closed from the inside with a rotational pericranial flap.

Uneventful healing with a slightly depressed scar after 6 months.

7.   Case example: Infection of allogenic graft, causing swelling and chronic headache

Chronic infection of the left frontal sinus after obliteration with a polymeric inlay causing swelling and chronic headache.

Exposure shows that the graft is embedded in granulation tissue.

After explantation and cleaning, the supraorbital rim is missing (arrow) and will be replaced with cranial bone.

The supraorbital rim was reconstructed with cranial bone and the defect obliterated with cortical cancellous bone chips.

The anterior table is replaced with a titanium mesh.

Alternatively, the anterior table can also be reconstructed with cranial bone. See case “partial obliteration”

8.   Case example: Exposure of a titanium mesh through the skin

This patient fell from a horse resulting in a extended frontal sinus and frontal bone fracture. Initial repair was done with PMMA which had to be removed due to an infection after one year. Secondary repair was done with a titanium mesh which was just laid onto the bone without fixation. After two years, the mesh began to perforate through the skin (arrow).

Wide-meshed titanium mesh floating on the defect without fixation.

Dead space below the mesh resulted in indentation of the skin (see also previous clinical photograph).

The defect in the frontal bone after removal of the mesh. The underlying dura (see arrow) is covered by thick scar.

Reconstruction of the defect was done with split cranial bone (outer table) taken as a full-thickness graft from the posterior half of the skull. The donor site defect was reconstructed with internal table.

Uneventful healing after 3 months. Note the thinning of the skin of the right forehead due to the taking of pericranial flap during initial repair.

9.   Case example: Osteomyelitis of the supraorbital rim with fistulization

This patient sustained a motor vehicle accident with a right frontal sinus and cranial base fracture requiring cranialization of the frontal sinus. Ten years after the accident, recurrent fistulization in the area of the glabella occurred. Despite several revisions using a local incision fistulization did not stop.

CT shows osteomyelitis and partial resorption …

… of the right supraorbital rim.

Intraoperative view after resection of the affected supraorbital rim.  Due to previous cranialization of the frontal sinus, a formal craniotomy was done to protect the dura.

The supraorbital rim was reconstructed with full thickness cranial bone taken from the posterior part of the skull.

Postoperative x-rays demonstrating …

… anatomical reconstruction of the supraorbital rim.

Postoperative clinical view. Elimination of the osteomyelitis allows for spontaneous healing of the fistula.

10.   Operative techniques: Transnasal endoscopic approach

Indications

Recent advances in endoscopic equipment and techniques (frontal sinus instrumentation, navigation, intraoperative CT) has greatly expanded the scope of access for endoscopic sinus surgeons. The preferred technique for treatment of paranasal sinus mucoceles is endoscopic drainage into the nasal cavity. If a mucocele can be drained into the nasal cavity there is no need for any further intervention. The mucocele simply becomes an accessory sinus. This avoids the need for external incisions, hardware application, or bone grafting. Frontal sinus endoscopic surgical techniques are among the most difficult endoscopic sinus procedures and should only be attempted by those comfortable doing them.

Limitations

Mucoceles inaccessible through the paranasal sinuses can not be accessed via an endonasal approach. Furthermore, mucoceles associated with contaminated hardware/implants generally can not be managed endoscopically.

Technique

A complete review of endoscopic surgical technique is beyond the scope of the Surgery Reference. However, general principles for endoscopic drainage of paranasal sinus mucoceles will be covered.

Most patients will require an endoscopic ethmoidectomy and possible maxillary antrostomy. Mucoceles emanating from the frontal sinus usually enlarge the sinus ostia making access less challenging. This illustration demonstrates a frontoethmoid mucocele displacing the orbital content inferiorly. Dehiscence into the anterior fossa is not a contraindication for transnasal endoscopic drainage.

A complete ethmoidectomy has been performed to allow for drainage of the mucocele. It is important to completely remove all ethmoid air cells. This minimizes the risk of recurrent obstruction and mucocele formation.

Resection of the bone on the inferomedial aspect of the mucocele provides a pathway for drainage of the mucocele into the nose. Intraoperative navigation assists the surgeon to more safely enlarge the opening without violating the orbital or intracranial cavities. The opening should be made as large as possible to minimize the risk of postoperative stenosis and obstruction, which can result in recurrent mucocele formation.

Case example I

A 60 year old female with frontoethmoid mucocele with proptosis, hypophthalmos, in an only seeing eye. The mucocele has also resulted in:

A bony orbital deformity

Globe compression and deformity

While there appears to be very limited access from the nasal cavity, this is quite adequate for transnasal endoscopic drainage of the mucocele.

Endoscopic photograph demonstrating decompression of the mucocele and suctioning of its contents.

Endoscopic transnasal view  from the nose into the mucocele.

Two years postoperatively, the mucocele cavity continues to drain and be well aerated. The bony deformity has also improved significantly.

The hypophthalmos and proptosis have resolved.

Case example II

70 year old male with posttraumatic frontoethmoid mucocele, hypophthalmos and exophthalmos.

Coronal CT scan of the same patient.

Postoperative CT scan demonstrating complete left ethmoidectomy and drainage of the mucocele. (Note: Septal perforation seen on CT scan was present prior to endoscopic mucocele decompression.