Introduction
The lateral skull base is comprised predominantly of the dense, pyramid-shaped petrous temporal bone. Fractures of the petrous temporal bone comprise approximately 20% of all skull fractures. Given the density of the petrous temporal bone, fractures are caused by high-impact trauma and are nearly uniformly associated with traumatic brain injury (TBI). In addition, 8%–29% of temporal bone fractures are bilateral, resulting in significant morbidity. ,
These fractures are typically caused by direct impact and compression mechanisms and, historically, have been classified as either transverse or longitudinal depending on the orientation of the fracture along the long axis of the temporal bone. More recent classification, however, has focused on the relationship of the fracture to the otic capsule as this represents a more clinically relevant distinction. In this scheme, fractures are either otic capsule sparing (OCS) or otic capsule disrupting (OCD). OCS fractures are more common, comprising approximately 95% of fractures, and typically result from direct impact on the temporoparietal convexity. Resultant fractures are through the posterior wall of the external auditory canal (EAC), mastoid air cells, middle ear, mastoid tegmen, and tegmen tympani. As a result, OCS injuries are associated with conductive or mixed hearing loss. In contrast, OCD fractures are typically from impact to the occiput with a fracture line from the foramen magnum through the petrous pyramid. These fractures can involve the jugular foramen, internal auditory canal, and foramen lacerum. OCD fractures lead to an obligate, often profound, and sensorineural hearing loss (SNHL) ( Fig. 9.1 ) .
Fractures of the lateral skull base are a source of significant morbidity. They can lead to cerebrospinal fluid (CSF) leak, facial nerve injury, meningitis, hearing loss (both conductive and sensorineural), and cerebrovascular injury. As such, early recognition is important to allow for appropriate management.
Clinical evaluation and diagnosis
Temporal bone fractures are typically the result of high-impact trauma. Often these fractures occur in patients who also have TBI and polytrauma. Therefore, it is common for temporal bone fractures to be initially diagnosed on a CT of the head. A temporal bone fracture should also be suspected in an awake posttrauma patient with facial weakness, dizziness, or hearing loss, or in an obtunded posttrauma patient with ecchymosis over the mastoid prominence (Battle’s sign) or otorrhea.
The physical exam is critical for acute diagnosis and management of these fractures. Otoscopy should be performed on any patient with a suspected fracture. Evaluation should begin with inspection of the external ear. Superficial lacerations will often heal without intervention. Circumferential lacerations of the EAC, however, may lead to stenosis in the future and should be repaired. The canal should also be inspected for brain parenchyma (rare) and CSF leak (more common). The integrity of the tympanic membrane (TM) should be assessed. The most common findings are hemotympanum if the TM is intact, and bloody otorrhea if the TM is perforated. Similarly, in the case of a CSF leak, otorrhea will be present if the TM is perforated, but if the membrane is intact, the fluid drains through the eustachian tube producing rhinorrhea. Pneumatic otoscopy should be deferred in the acute setting to avoid introduction of air and bacteria into the subarachnoid space.
Evaluation and documentation of facial movement is also imperative in the acute setting as it has significant prognostic value . By necessity, facial movement evaluation is often delayed, however, as patients may be intubated and unable to participate in an examination or other injuries may take priority. Those patients who cannot be examined immediately should be considered to have indeterminate onset of facial weakness. The House–Brackmann scale is a simple and consistent grading scale that can be utilized for long-term follow-up. Patients with immediate, acute-onset complete facial paralysis have a much worse prognosis for recovery than those with delayed-onset weakness. Recovery of incomplete facial paralysis is seen in nearly 100% of cases. , , ,
Hearing should also be tested at bedside with a 512-Hz tuning fork. The Rinne and Weber tests can help differentiate conductive hearing loss from SNHL. Audiometry is typically delayed for several weeks after initial trauma to allow for resolution of middle ear fluid unless the patient requires an urgent surgical intervention.
Disruption of the otic capsule can present with vertigo and nystagmus. For that reason, an examination of extraocular movements should be performed to assess for nystagmus in addition to cranial nerve III, IV, and VI palsies. An abducens palsy is common in TBI and can be associated with temporal bone fractures, especially fractures extending into the clivus.
High-resolution temporal bone CT is not routinely necessary unless patients develop persistent CSF leaks, hearing loss, or facial weakness. It should also be obtained prior to any planned surgical intervention. CT angiography should also be considered in the setting of temporal bone fractures as the petrous segment of the internal carotid is at risk for injury as are the transition points between the relatively mobile cervical and petrous segments and the petrous to lacerum segments.
Management and outcomes
Management of lateral temporal bone fractures hinges on the indications for surgical intervention. In general, early surgery should be considered for open, depressed squamous temporal fractures or any mass occupying lesions with a poor neurologic exam, such as a large temporal lobe contusion or an epidural hematoma. The goal of acute surgical intervention is preservation of neurologic function and decompression of the brainstem. In contrast, delayed surgical intervention is reserved for persistent CSF leaks and facial nerve decompression.
Cerebrospinal fluid leak
CSF leak occurs in approximately 17% of temporal bone fractures. , , It significantly increases the patient’s risk of meningitis and ensuing morbidity. Evidence of a CSF fistula may be present initially on examination, but also commonly develops several days following an injury as posttraumatic soft tissue edema resolves. It may present as either clear otorrhea or rhinorrhea depending on the integrity of the TM. In OCS fractures, the CSF fistula typically occurs through a fracture in the tegmen tympani or mastoideum, whereas in OCD fractures, the leak typically results from injury to the posterior fossa dura creating a direct fistula from the posterior fossa subarachnoid space into the middle ear via the otic capsule. The leak can be confirmed as CSF by evaluating the fluid for the presence of Beta2-transferrin, which is only present in CSF, perilymph, and aqueous humor.
Initially, the treatment for a CSF fistula should be conservative, using measures to decrease intracranial pressure and diminish any pressure gradient as a fibrous layer forms to seal the dural defects. Such measures include elevation of the head of bed, stool softeners, avoidance of sneezing, and nose blowing as well as avoiding situations requiring the equivalent of a Valsalva maneuver. Temporary CSF diversion with repeated lumbar punctures or a lumbar drain can also be employed. With conservative management, 57%–85% of CSF fistulae will resolve within 1 week of initial injury. , , , ,
After 1 week, the risk of meningitis increases significantly, ranging from 88% to 100% among those with persistent CSF leaks. , , Among these patients, Pneumococcus , Streptococcus , and Haemophilus influenzae are the most common pathogens. With such a high incidence of meningitis, persistent CSF leak is an indication for operative repair. To facilitate surgery, further investigation should be directed toward identifying the site of the leak. A high-resolution CT of the temporal bone is able to locate the site of CSF egress in 70% of cases. If the CT is inconclusive, then an intrathecal fluorescein evaluation can be performed to localize the site of the leak. Surgical repair should ensue after the site of the leak has been identified.
The surgical approach for repair of a CSF fistula is determined by the site of the leak and the hearing status of the patient. In OCD fractures with profound SNHL, a complete mastoidectomy with removal of ossicular chain, obliteration of the eustachian tube, and oversewing of the EAC is recommended to treat the leak. The approach for CSF leak repair in OCS fractures with salvageable hearing, on the other hand, is dictated by the location of the leak. The most common site of leak is the tegmen tympani. For these locations, a middle fossa craniotomy and a temporalis fascia flap overlay are the approaches of choice. For other sites of leak, a transmastoid, labyrinth-sparing approach allows for repair of the fistula while preserving hearing. ,
Due to the risk of meningitis resulting from CSF fistula, consideration has been given to the use of prophylactic antibiotic therapy. Historically, practice has varied widely regarding the use, duration, and agents used for prophylactic therapy. However, a metaanalysis performed in 2011 by Ratilal et al. found no reduction in the frequency of meningitis, all-cause mortality, meningitis-related mortality, or need for surgical correction between antibiotic use and nonuse in those with a CSF leak. Therefore, in the absence of concern for meningitis, antibiotic prophylaxis is not generally recommended for those with a CSF leak.
Facial nerve injury
Facial nerve injury occurs in 6%–7% of temporal bone fractures. Of those with facial nerve injury, 27% will initially present with facial weakness, while the other 73% will develop delayed-onset facial weakness within 1–16 days after the injury. Most patients will develop partial facial weakness, with only 25% presenting with acute-onset complete paralysis (i.e., House–Brackman 6 facial weakness). Regardless of severity and timing of weakness onset, the initial treatment should be with 7–14 days of systemic glucocorticoid treatment.
Delayed facial weakness and incomplete weakness are associated with better long-term outcomes than acute-onset, complete facial paralysis. Ninety-four percent of delayed facial weakness patients completely recover, and up to 100% of patients with incomplete facial weakness will completely recover. , , Therefore, surgical decompression of the facial nerve is reserved for acute-onset, complete facial weakness with poor prognosis for recovery. Prognosis is determined electrophysiologically, using electroneurography (ENoG) and voluntary electromyography (EMG). ENoG measures the compound muscle action potential generated by an electrical stimulus at the stylomastoid foramen. These muscle action potentials are the result of synchronous discharge of multiple viable nerve fibers, and decreased amplitudes suggest Wallerian degeneration. Voluntary EMG measures the motor response via needle electrodes when a patient attempts to make facial muscle contractions. EMG is typically used in patients for whom ENoG has demonstrated >90% degeneration to evaluate for active motor units that may be too asynchronous in their activity to produce a compound action motor potential. The presence of asynchronous active motor units suggests recovering nerve fibers and portends a better prognosis. Electrophysiologic testing should be delayed for at least 3 days to allow Wallerian degeneration to occur because patients with complete nerve disruption will retain distal stimulability for 3–5 days after initial injury. Moreover, testing is not typically performed after 14 days as those with >90% degeneration after 2 weeks do not show favorable response to surgical intervention, while those who have not met the 90% degeneration threshold have a high chance of recovery.
The most common site of injury is the perigeniculate facial nerve in the fallopian canal. For OCS fractures, surgical approach is typically transmastoid, supralabyrinthine to expose the distal labyrinthine segment down to the mastoid segment of the facial nerve and to decompress it in the fallopian canal. Alternatively, a middle fossa craniotomy can be performed with direct decompression of the perigeniculate facial nerve by identifying the greater superficial petrosal nerve and following it proximally to the geniculate ganglion. For OCD fractures, as a consequence of the SNHL, a translabyrinthine approach can be used to decompress the facial nerve. In all cases, the goal is to remove any bony fragments compressing the perineurium or to repair a transected nerve. , In cases of facial nerve transection, primary anastomosis between facial nerve ends has the most favorable results in motor outcomes. However, when the facial nerve is too damaged to repair primarily, then a “cable graft” can be performed. In this procedure, a section of donor nerve is harvested and used as an interposition graft to restore the continuity of the facial nerve. Common donor nerves include the greater auricular nerve, sural nerve, and the medial and lateral antebrachial cutaneous nerves. Alternatively, a hypoglossal-facial anastomosis can be performed. , , In cases where the facial nerve does not recover, then facial reanimation can be performed in a delayed fashion.
The most important aspect of preventative care for a patient with facial weakness is eye protection. As the facial nerve recovers, the patient is at high risk for exposure keratitis and corneal abrasions, which can comprise vision. Artificial tears, ointment, and moisture chambers should be utilized. Lateral tarsorrhaphy can be utilized to augment eye closure in incomplete injuries. In complete paralysis, a gold weight should be considered in the upper eyelid.
Hearing loss
Hearing loss is common with temporal bone fractures. Depending on the fracture, it can be conductive, SNHL, or mixed. While OCS fractures can present with conductive or mixed hearing loss, OCD fractures are uniformly SNHL, which is the type that has the worst prognosis for recovery. As previously mentioned, an audiogram should be delayed for 4–6 weeks postinjury to allow for resolution of middle ear fluid.
Conductive hearing loss is typically secondary to middle ear effusion or hemotympanum but in up to 20% of patients can be due to ossicular chain disruption. For those with persistent conductive hearing loss lasting for longer than 6 months, an exploratory tympanotomy with possible ossiculoplasty can be considered. These patients may also benefit from hearing aids or amplifiers. Repair should not be attempted earlier because scar formation around the ossicular chain and resorption of middle ear fluid often resolves the hearing loss.
SNHL has a worse prognosis for recovery than conductive hearing loss. It can also occur in patients with TBI without temporal bone fractures. Surgical intervention is typically not indicated, but those with bilateral profound SNHL can be treated with cochlear implants.
Vertigo
Vertigo and dizziness are common with temporal bone fractures and TBI, in general. The most common type of vertigo is benign paroxysmal positional vertigo. The patient should initially be treated with vestibular rehabilitation. For most patients, the vertigo, and resultant nystagmus, will resolve within 4–6 weeks of initial injury. For patients with OCD fractures, vestibular rehabilitation may be required for a longer period of time.
Vascular injury
High-impact trauma to the head and neck region is associated with traumatic dissections to cerebral vasculature. These traumatic dissections are a nidus for clot formation and as a result place the patient at risk for stroke. Arterial transition points are particularly vulnerable to injury, including the entry of the cervical internal carotid artery into the petrous temporal bone. For this reason, any patient with lateral skull base trauma should also be considered for a CT angiogram of the head and neck to assess for arterial injury. Internal carotid artery dissection with at least 25% stenosis, pseudoaneurysm formation, or occlusion is typically treated with antiplatelets or anticoagulation.
Additional considerations
Patients who sustain an injury to the EAC or have undergone ear surgery are at increased risk for external canal stenosis and cholesteatoma formation, both of which can lead to impaired hearing. Cholesteatoma formation can occur following trauma by one of four possible mechanisms: skin epithelial entrapment in a fracture line, ingrowth of epithelium in an unhealed fracture line or disrupted TM, traumatic implantation of epithelium in middle ear, or trapping of skin epithelium medial to an EAC stenosis. Therefore, patients require continued, long-term monitoring after temporal bone fractures for cholesteatoma formation and EAC stenosis. If the patient develops EAC stenosis, then it is recommended to stent the stenosis or perform a canaloplasty to prevent cholesteatoma formation and augment hearing.
Conclusions
Petrous temporal bone fractures are caused by high-impact trauma and can result in significant morbidity. The most common complications are facial nerve injury, CSF leak, and hearing loss. The timing of onset of facial weakness and degree of injury is the most critical initial evaluation to determine next step in management. Overall, most complications can be managed conservatively with favorable outcomes. Following temporal bone fracture, patients require long-term monitoring for delayed cholesteatoma formation.
References
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