The skull base includes the frontal bone, the sphenoid bone, the temporal bone, and the occipital bone. A fracture in the skull base (otherwise known as a basilar skull fracture) must involve at least one of these bones and may involve all of them. Temporal bone fractures represent roughly 20% of all skull fractures. Risk factors include being male and under 21. The most common causes include motor vehicle accidents, falls, bicycle accidents, seizures, and aggravated assaults. Blunt trauma to the lateral surface of the skull (the squamous portion of the temporal bone) often results in a longitudinal fracture. A blow to the occipital skull may go through the foramen magnum and result in a transverse fracture of the temporal bone (Figure 59–1).
Types of temporal bone fractures. (A) Longitudinal fractures begin at the squamous portion of the temporal bone, run through the external auditory canal, and then turn anteriorly toward the foramen lacerum. (B) Transverse fractures begin from the foramen magnum, run through the otic capsule bone that surrounds the inner ear, and then turn anteriorly toward the foramen lacerum.
Longitudinal fractures involve the squamous portion of the temporal bone, follow the axis of the external auditory canal to the middle ear space, and then course anteriorly along the geniculate ganglion and eustachian tube, ending near the foramen lacerum. In a longitudinal temporal bone fracture, the otic capsule is spared. In contrast, transverse fractures course directly across the petrous pyramid, fracturing the otic capsule, and then extend anteriorly along the eustachian tube and geniculate ganglion. Longitudinal temporal bone fractures and transverse temporal bone fractures represent 80% and 20%, respectively, of temporal bone fractures.
Symptoms include hearing loss, nausea and vomiting, and vertigo. Clinical signs include Battle sign, which is a postauricular ecchymosis resulting from extravasated blood from the postauricular artery or mastoid emissary vein. The “raccoon” sign (periorbital ecchymosis) is associated with basilar skull fractures that involve the middle or anterior cranial fossa. Physical examination may demonstrate an external auditory canal laceration with bony debris within the canal. A hemotympanum is almost always identified. Cerebrospinal fluid (CSF) otorrhea or rhinorrhea may be seen. Tuning fork tests should always be performed on patients with a temporal bone fracture. The Weber tuning fork test radiates to the fractured ear if conductive hearing loss is present and radiates to the contralateral ear if sensorineural hearing loss is present. The presence or absence of facial nerve paralysis should be documented in all patients with temporal bone fractures.
After initial resuscitation in the emergency room, computed tomography (CT) scanning of the head is usually the first study performed on patients with head trauma. It is critical to rule out an intracranial hemorrhage, which may require urgent neurosurgical treatment. It is at this point that a temporal bone fracture is usually identified. High-resolution CT scanning of the temporal bone is valuable in delineating the extent of the fracture, but it is not required unless a complication is suspected (eg, otic capsule fracture, facial nerve injury, or CSF leak). Patients with a longitudinal fracture associated with hemotympanum, without nystagmus, without evidence of CSF leak, with a Weber tuning fork test that radiates to the affected ear, and with normal facial nerve function typically do not need a CT scan of the temporal bone. Angiography may be performed if there is significant hemorrhage from the skull base to rule out vascular injury, but this is uncommon.
Audiometry should be performed on all patients with a temporal bone fracture. However, this does not need to be done acutely in most cases. If clinical examination is consistent with conductive hearing loss and there is no evidence of otic capsule fracture, audiometric assessment can be performed several weeks after the injury, permitting time for the hemotympanum to resolve. If the otic capsule is fractured, there is a high likelihood of permanent complete sensorineural hearing loss and there is no treatment available to alter this prognosis. Urgent audiometry may be considered if stapes subluxation into the vestibule has occurred and surgery to repair a perilymph fistula is planned.
Facial nerve testing should be performed if a delayed, complete facial palsy occurs. The rationale is to identify patients with >90% degeneration of the facial nerve, because these patients have poorer recovery of the function and may benefit from surgical decompression. The nerve excitability test is performed by placing the two probes of a Hilger nerve stimulator across the stylomastoid foramen and slowly turning up the current until a facial twitch is just barely visible. This is the stimulation threshold of the facial nerve. A 3.5-mA difference between the injured and uninjured sides correlates with a > 90% loss of neural integrity.
Alternately, electroneuronography can be performed by a neurophysiologist. This involves stimulating both facial nerves with equal currents while simultaneously measuring the evoked myogenic potential in the muscles of facial expression. If the amplitude of the ipsilateral evoked potential is < 10% of that from the contralateral side, >90% loss of neural integrity has occurred. Neither of these tests is accurate within 3 days of the injury because it takes about 72 hours for nerve fibers distal to the site of the injury to degenerate. Nonetheless, surgical decompression of delayed facial paralysis remains controversial.
Conductive hearing loss is most commonly due to hemotympanum, but may also represent a tympanic membrane perforation or ossicular discontinuity. The most common form of ossicular discontinuity after temporal bone trauma is incudostapedial joint dislocation. The second most common is incudomalleolar joint dislocation (Figure 59–2). In addition, ossicular fixation may occur several months after the trauma if new bone formation at the line of the fracture fuses to the ossicular chain.
Axial computed tomography scan of a patient who sustained a longitudinal temporal bone fracture several months previously. This patient had a 60-dB conductive hearing loss with a normal tympanic membrane on physical exam. (A) The inferior cut demonstrates the line of the fracture. (B) The superior cut shows dislocation of the malleus-incus joint. Note that the fracture runs directly along the geniculate ganglion, but the patient did not have facial nerve dysfunction.
Sensorineural Hearing Loss and Vertigo
These complications are found in patients who sustain a transverse temporal bone fracture with otic capsule involvement (Figure 59–3). Pneumolabyrinth (air in the inner ear) is often noted by CT. An audiogram usually demonstrates a complete sensorineural hearing loss in the affected ear. Acutely, clinical examination also reveals nystagmus, which is consistent with a unilateral vestibular deficit. Sensorineural hearing loss can also be sustained without otic capsule fracture if a labyrinthine concussion, traumatic noise exposure, or blast injury occurs. This is thought to involve tearing of the cochlear membranes and/or trauma to the hair cell epithelium due to the rapid acceleration and deceleration forces within the inner ear. These injuries can manifest either as a high-frequency hearing loss, atemporary threshold shift in their hearing that resolves, or a permanent and complete sensorineural hearing loss.
Axial computed tomography scan of an 8-year-old child who sustained a transverse temporal bone fracture. This patient had nystagmus and a complete sensorineural hearing loss. His facial nerve function was normal. (A) The inferior cut demonstrates the line of the fracture that extends through the dense, white bone of the otic capsule. (B) The superior cut shows that the fracture extends to the facial nerve canal.
Facial nerve palsy occurs in 20% of longitudinal temporal bone fractures and 50% of transverse temporal bone fractures. The most important clinical feature to identify is whether the facial nerve palsy was of delayed or immediate onset. Patients with delayed-onset palsy present to the emergency room with normal facial nerve function that slowly worsens over the next several hours to days. This is thought to represent edema within the facial nerve without disruption of neural integrity. In contrast, immediate facial nerve injury is highly suggestive of facial nerve transection. Unfortunately, it is common to have an undetermined onset time of facial nerve palsy because patients with temporal bone fractures and facial nerve palsy typically have many other life-threatening issues that are being dealt with at the time of the initial evaluation. These patients are often comatose and therefore difficult to examine.
There is a 2% incidence of CSF leak in all skull fractures and a 20% incidence in temporal bone fractures. CSF leaks usually start within the first 48 hours of the trauma and are noted as clear fluid emanating from the ear or nose. Straining, standing up, or bending over worsens the CSF leak. If clear fluid emanating from the nose or ear is suggestive of a CSF leak, the fluid can be collected and sent for Î²2 transferrin testing. Î²2 transferrin is a protein found only in CSF.
Posttraumatic encephalocele can result if a large defect in the floor of the middle cranial fossa occurs. Dura and temporal lobe brain can herniate down into the middle ear and mastoid. This can sometimes be visible on otoscopic examination of the ear as a white mass with blood vessels behind the tympanic membrane. A CSF leak can occur in combination with an encephalocele.
A perilymphatic fistula can occur after a fracture of the otic capsule or stapes subluxation of the oval window. It manifests as fluctuating vertigo and sensorineural hearing loss. This entity is fully described later in this chapter.
A hemotympanum resolves spontaneously within 34 weeks of the injury with no sequelae. Traumatic tympanic membrane perforations have an excellent chance of healing spontaneously. Within 1 month, 68% are healed; within 3 months, 94% are healed. If the perforation has not healed by 3 months, a paper-patch myringoplasty can be attempted in the office. This should be performed only if the perforation is quite small (<25%) and does not involve the margins of the eardrum and if the middle ear mucosa appears uninfected and dry. The edges of the perforation are freshened with a Rosen needle and a paper patch (cigarette paper or a Steri-Strip) is placed over the perforation.
If the perforation is large or has failed an attempt at paper-patch myringoplasty, the patient should be taken to the operating room for a standard tympanoplasty. The ossicular chain should also be explored to verify that it is intact during this procedure. A patient with a normal tympanic membrane and persistent conductive hearing loss probably has ossicular chain discontinuity. A middle ear exploration should be done through the canal by raising a tympanomeatal flap and carefully inspecting and palpating the ossicles. Ossicular chain reconstruction is based on the site of the injury.
The treatment of delayed-onset palsy is based on conservative, nonsurgical management. It is expected that 94% to 100% of these patients will have complete and full recovery of their facial nerve function. However, patients with > 90% degeneration of neural integrity have been shown to have poor recovery. Presumably, the nerve is swollen within the bony fallopian canal, compressing itself within this confined space and therefore causing permanent injury to the nerve fibers.
The management of patients with > 90% degeneration is controversial. Although some neurotologists recommend facial nerve exploration and decompression, others recommend watchful waiting. In contrast, there is no controversy about patients with immediate-onset facial palsy. These patients should undergo facial nerve exploration as soon as the patient is medically stabilized. Human studies have not proved that early surgery improves the long-term facial nerve outcome, but animal studies suggest that intervention within 21 days of facial nerve transection is beneficial.
The exploration of posttraumatic facial nerve palsy is based on two routes. If the patient has normal hearing, a combined middle fossa-transmastoid facial nerve exploration is performed (Figure 59–4). This includes a subtemporal craniotomy with delineation of the facial nerve within the internal auditory canal from the porus acousticus internus to the geniculate ganglion. A mastoidectomy is also performed to explore the facial nerve from the middle ear to the stylomastoid foramen. If the patient has a complete sensorineural hearing loss, a translabyrinthine facial nerve exploration and repair can be undertaken (Figure 59–5). This approach allows for complete exposure of the facial nerve from the porous acousticus to the stylomastoid foramen completely through the mastoid.
The combined middle fossa-transmastoid approach. This approach is used for facial nerve exploration in patients with normal hearing. The middle fossa exposure permits visualization of the nerve from the brainstem to the geniculate ganglion, whereas the transmastoid route exposes the nerve from the geniculate ganglion to the stylomastoid foramen. In this example, an interpositional facial nerve graft has been placed within the vertical segment of the facial nerve.
The translabyrinthine approach. This approach is used for facial nerve exploration in patients with complete sensorineural hearing loss and allows complete exposure of the nerve through one opening. In this example, a primary facial nerve anastomosis has been performed.
Injuries are most commonly located in the area of the geniculate ganglion. If an intraneural hematoma is identified, the epineurium should be carefully opened and the hematoma evacuated. If bony fragments are impinging upon the nerve, these can be carefully removed as well. If there is an obvious fracture of the facial nerve, the two ends of the facial nerve should be freshened and anastomosed. If the segment of missing nerve is too long to be easily anastomosed without tension, an interposition nerve graft should be used from the greater auricular or sural nerve. If no pathology is visualized, the act of opening the bony canal of the facial nerve should allow adequate decompression and permit swelling of the nerve without impingement. The epineurium does not need to be incised.
Cerebrospinal Fluid Leak and Encephalocele
Eighty percent of posttraumatic CSF leaks close spontaneously after 7 days, and the risk of meningitis is quite low (3%) within this time period. Thus, medical treatment is attempted initially. This includes head elevation, stool softeners, acetazolamide (to decrease CSF production), and the placement of a lumbar drain. Patients with intracranial hemorrhage who have undergone craniotomy often already have an intraventricular drain in place, in which case a lumbar drain is not needed. Short-term antibiotics have been shown to be useful in preventing meningitis. The most common organisms that cause meningitis in this situation are Pneumococcus, Staphylococcus, Streptococcus, and Haemophilus influenzae. If the CSF leak persists for more than 7–10 days, the risk of meningitis increases dramatically (>20%) and surgical repair of the CSF leak should be performed. This situation is most common in patients who sustain a transverse temporal bone fracture with CSF leaking through the otic capsule. Otic capsule bone does not heal with new bone formation but by fibrous union, and this is often not strong enough to contain CSF.
An encephalocele should always be surgically repaired. If the patient has normal hearing, the repair of either a persistent CSF leak or an encephalocele is via a combined middle fossa craniotomy-transmastoid approach with dural repair and skull base reconstruction. In a patient with no useful hearing, obliteration of the ear with an abdominal fat graft, plugging of the eustachian tube, and closure of the ear canal can be performed through the mastoid alone.
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