Traumatic Facial Nerve Management
Trauma is second to idiopathic facial paralysis (Bell palsy) as the most common cause of facial paralysis. The course of the facial nerve is complex with intracranial, intratemporal, and extratemporal segments. The nerve is at risk for injury along any of these segments from external, surgical, or iatrogenic trauma. Management of facial nerve trauma is often challenging as spontaneous recovery cannot be predicted and is often satisfactory without intervention. The two most important factors predicting recovery and potential intervention include onset and degree of paralysis. In this chapter, the evaluation and management of traumatic facial nerve paralysis is discussed.
External Trauma
Temporal bone fractures occur in 4.4–9.4% of patients presenting with head injuries and in up to 40% of patients with basilar skull fractures, especially those associated with motor vehicle accidents.1,2 Approximately 14–22% of patients with skull fractures will have an associated temporal bone fracture.3 Patients with temporal bone fractures often present with other severe and life-threatening issues that appropriately take precedence with respect to diagnosis and management.
Evaluation
A careful history and physical exam can often confirm the presence or absence of hearing loss, vertigo, facial paralysis, cerebrospinal fluid leak, and in some cases a vascular injury in patients with a basilar skull fracture. Patients with otorrhea or hemotympanum will at a minimum have some conductive hearing loss. Fractures that traverse the otic capsule will almost always result in a significant sensorineural hearing loss. A simple tuning fork test will confirm the type of hearing loss present, which is of critical importance if surgery is being considered to address a persistent cerebrospinal fluid leak or facial paralysis.
Evaluation of facial nerve function during the initial examination is crucial when predicting recovery and the need for surgical intervention. In the setting of external trauma, facial function should be assessed as soon as possible. Eyewitness accounts from the scene of the accident should be interpreted with caution; however, useful information may be obtained. Many patients have severe concomitant injuries and arrive intubated and sedated, making the initial evaluation of facial function difficult. Painful stimuli such as a sternal rub or pressure under the superior orbital rim may stimulate facial movement. Despite the examiner′s best efforts, often an adequate exam may not be possible and the patient will need to be reassessed once his or her condition has stabilized.
Onset and Degree of Paralysis
Sudden and Complete
Facial paralysis that is sudden and complete portends a worse prognosis with only 36% of patients making a full recovery in a recent large meta-analyses.4 The challenge is to differentiate which patients will have poor recovery from those that will experience good recovery. A combination of imaging and electrical testing will determine if surgical exploration is warranted.
Delayed or Incomplete
Delayed paralysis confirms the continuity of the facial nerve and occurs due to edema of the facial nerve in the fallopian canal, especially around the meatal foramen.5 If the paresis does not progress to complete paralysis, management is always expectant and full recovery is almost certain. If the paralysis progresses to complete, electrical testing may be performed. Surgical decompression is rarely indicated because > 90% of patients will have full recovery of facial function.3,6–8 Surgery may be considered if electric testing places the patient in a poor prognostic category. Many surgeons use the same electrophysiological criteria as in Bell palsy when determining if facial nerve decompression is warranted (see Chapter 11).
Unclear Onset
Often the onset of paralysis cannot be determined due to confounding factors such as neurological status or other life-threatening injuries. In these cases, the onset of paralysis is questionable and these patients should be classified as acute onset. Electrical testing is paramount in these circumstances if surgical exploration is considered.
Classification of Temporal Bone Fractures
Temporal bone fractures have historically been categorized according to their orientation with respect to the petrous ridge (longitudinal, oblique, transverse).9 Defining the fracture according to involvement of the otic capsule has become the preferred classification scheme as it has been shown to be a better prognostic indicator of intratemporal complications including facial paralysis.2 Otic capsule– sparing fractures occur far more frequently (> 94%) than fractures that traverse the otic capsule (< 6%).2,3 Facial paralysis is twice as common in otic capsule–involving fractures where the tympanic facial nerve is the most commonly injured segment.2,10 Fig. 12.1 demonstrates an otic capsule fracture crossing the common crus and medial vestibule resulting in a facial paralysis. Six percent to 14% of otic capsule–sparing fractures are associated with facial paralysis that usually involves the perigeniculate portion of the facial nerve.2,3,10
Diagnostic Testing
Thin-cut computed tomography (CT) is the mainstay of radiographic assessment of the patient with traumatic facial nerve injury. CT can demonstrate a skull base fracture in almost all cases. Images must be carefully examined to make sure all fracture lines are identified as multiple fractures are often present. While many fractures conform to one of the types described previously (“longitudinal” or “transverse”), others do not. Most fractures associated with facial paralysis will involve the area of the geniculate ganglion and/or labyrinthine segment of the facial nerve. Fig. 12.2 demonstrates a longitudinal fracture affecting the perigeniculate region resulting in facial paralysis. If facial paralysis is complete, an attempt should be made to assess the extent of displacement and/or fragmentation of the fallopian canal to estimate the likelihood that the nerve is transected or that the facial nerve is compressed by bone fragments. In the face of complete facial paralysis and/or a poor prognosis from electrodiagnostic testing, image findings of severe injury as suggested by the CT scan would encourage surgical exploration.
If the fracture involves the petrous carotid canal, a CT or magnetic resonance angiogram is essential. The most common location for a basilar skull fracture to involve the carotid canal is at the lacerum-cavernous junction.11 An unrecognized carotid injury may result in stroke or death if not promptly diagnosed.
If the paralysis is of immediate onset, electrodiagnostic testing can be very useful in determining the extent of injury. While both electroneuronography (evoked electromyography) and maximal stimulation testing can provide useful information, electroneuronography is more precise and provides an objective record of the evaluation. Absent response on the injured side on electroneuronography suggests transection of the nerve. A full description of electrodiagnostic testing can be found in Chapter 5. Electrodiagnostic test results should be considered together with CT findings.
Management
Several controversies exist with respect to the management of facial paralysis secondary to a temporal bone fracture. The timing and degree of facial paralysis is of critical importance with respect to prognosis and management. Patients with immediate onset complete paralysis with poor prognostic electrodiagnostic testing are candidates for surgical exploration of the facial nerve. Most reports agree that surgical intervention 14 days after the injury is rarely indicated; however, several authors suggest that late facial nerve exploration may have some benefit in cases where an impinging bone fragment or transection of the nerve is suspected.4,12,13 The surgical approach for facial nerve exploration primarily depends on the hearing status and location of the fracture. Patients with anacusis or otic capsule–involving fractures are typically managed with a translabyrinthine approach.12 A middle fossa possibly combined with a transmastoid approach is utilized in patients with intact hearing and fractures that involve the perigeniculate and more distal segments of the facial nerve.12
Outcomes
Facial paralysis resulting from blunt trauma has a favorable outcome in most cases.4 A recent review of the literature demonstrated that 82% of patients with a partial paralysis who were observed achieved complete recovery. Administration of steroids seemed to result in improved outcomes over those patients observed, resulting in normal function in 95% of patients with partial facial paralysis. With respect to onset of paralysis ∼80% of patients with delayed paralysis who underwent no intervention recovered normal function. It is well known that traumatic complete facial paralysis has a worse outcome than in those individuals with partial or incomplete paralysis. In a pooled series of 480 patients with complete paralysis, 57% of patients who were observed, 44% of the patients who were administered steroids, and 21% of patients undergoing decompression demonstrated complete recovery of function. Complete lack of recovery was observed in 1.7% of patients as compared with 10% of patients undergoing decompression. No patients who were administered steroids developed a complete long-term facial paralysis.4
Extratemporal Facial Nerve Trauma
The most common cause of extratemporal facial nerve injury is from penetrating trauma or iatrogenic injury. A careful examination of all branches of the facial nerve is warranted in cases of external penetrating facial trauma. Ideally, penetrating facial injuries with resultant facial weakness should be explored immediately, provided the patient is medically stable. Transected branches can usually be identified through the existing facial laceration. A facial nerve integrity monitor can be used to identify distal facial nerve branches if the exploration can be performed within 72 hours from the time of injury prior to the onset of wallerian degeneration. The main trunk of the facial nerve can be identified at the stylomastoid foramen or in the mastoid fallopian canal if localization of the proximal branches is difficult. The nerve can then be traced to the pes anserinus and from there to the proximal transected end of the facial nerve.
Primary repair of the facial nerve without mobilization is associated with improved outcomes as opposed to rerouting or grafting. Improved outcomes are also seen when fewer branches are injured.14