Intratemporal Bone Trauma Treatment & Management

Updated: May 31, 2018
  • Author: Noah Massa, MD, FRCSC; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Treatment

Medical Therapy

Patients with traumatic facial paralysis are often treated empirically with a short course of oral steroids. In contrast to idiopathic facial paralysis or Bell palsy, no studies confirm or dispute the utility of steroid treatment after traumatic facial paralysis. The potential risks of using corticosteroids in a patient with multiple trauma and possible risk of infectious complications must be weighed against the unknown probability for benefit in decreasing the risk of permanent facial paralysis. A typical course of high-dose prednisone is 1 mg/kg for up to 10 days followed by a tapering regimen.

Proper eye care with use of artificial tears and night patching should be implemented as long as eye closure is impaired.

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Preoperative Details

Because multiple injuries are possible at any point along the course of the facial nerve, it may have to be entirely decompressed from the IAC to the stylomastoid foramen. Localization of the site of injury should be attempted preoperatively.

The choice of surgical approach is primarily based on whether the patient has a loss of auditory or vestibular function allowing sacrifice of the labyrinth. Needle EMG may be used intraoperatively early after an injury has occurred to test integrity of the facial nerve. [11, 12, 13]

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Intraoperative Details

Patients with intact auditory and vestibular function should undergo exploration of the facial nerve by means of a combined approach involving the mastoid, middle ear, and middle cranial fossa under general anesthesia. Minor variations in technique are used. The following discussion provides a general overview.

After a standard postauricular incision is made, complete mastoidectomy is performed. The nerve is exposed throughout its vertical segment to the stylomastoid foramen. General surgical principles involve the use of diamond-tipped burrs of various sizes and copious irrigation to remove bone and prevent additional thermal trauma to the facial nerve. The final thin layer of bone overlying the nerve is removed with blunt elevators. The benefit of performance of neurolysis of the nerve sheath to decompress the nerve is debatable.

The tympanic cavity is approached by means of the facial recess, and assessment of the integrity of the ossicles is then possible. Visualization of the tympanic course of the facial canal is also undertaken. Bone overlying the tympanic segment is removed to the cochleaform process. Because the canal bone is thin, only the smallest diamond burr is used. Removal of the incus and amputation of the head of the malleus is likely necessary to expose the tympanic segment of the nerve.

A middle cranial fossa approach is undertaken to expose the labyrinthine portion of the facial nerve. A posteriorly based trap-door incision is made above the ear as a separate cut or as an extension of a postauricular incision. The skin is elevated to expose temporal muscle fascia, which is harvested for later closure of dural defects. The muscle and underlying periosteum are then elevated.

A temporal bone flap is then elevated. A properly positioned flap is one in which the base parallel to the middle cranial fossa floor, with two thirds of the square anterior and one third posterior to a line drawn vertically through the EAC. Great care must be exercised when the flap is elevated to avoid injury to branches of the middle meningeal artery, which are often embedded in the inner table. Dural elevation from the floor of the middle cranial fossa proceeds from posterior to anterior to avoid avulsion injury to the geniculate ganglion. Elevation continues until the petrous ridge is reached and until the arcuate eminence and greater superficial petrosal nerve are identified.

Bone dissection begins with exposure of the greater petrosal nerve and geniculate ganglion until connection is made with the previous tympanic dissection. Drilling then continues posteriorly to the arcuate eminence to expose otic capsule bone and the blue line of the superior semicircular canal. The IAC is identified and exposed in the bifurcation of the angle between the superior semicircular canal and the greater superficial petrosal nerve. The labyrinthine segment of the facial nerve is followed to the geniculate ganglion. Careful dissection is essential to avoid the superior semicircular canal and the basal turn of the cochlea in this region.

Once entirely exposed, the nerve can be examined and tested for integrity or injury. Neurolysis and/or nerve repair may be performed at this stage, depending on the degree of injury to the facial nerve. If primary repair is not possible in the case of nerve transection, a rerouting procedure or interpositional grafting can be used.

A piece of bone flap is used to cover defects made in the tegmen tympani and IAC to prevent herniation of the temporal lobe into the middle ear. In addition, the previously harvested temporalis fascia is used to seal any dural defects that were created. Repositioning of the temporal bone flap and layered closure are then accomplished.

Exploration of the facial nerve by means of the translabyrinthine approach is performed when hearing and vestibular function is lost. This approach offers access to the entire intratemporal course of the facial nerve with substantially decreased morbidity.

After a postauricular incision is made, the mastoid and tympanic portions of the facial nerve are exposed as described above. Complete labyrinthectomy follows to expose the IAC.

Blunt removal of bone over the nerve begins at the IAC by extending along the labyrinthine segment to the geniculate ganglion. Distal dissection to the stylomastoid foramen is then performed. Lastly, fascia and muscle may be used to fill the middle ear by plugging the auditory tube orifice, and the mastoid is obliterated with harvested abdominal fat.

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Follow-up

Patients and families must be counseled that improvement in function may not be realized for as long as a year after surgery. In the case of repaired transection injuries, initial recovery may occur at 6 months with continued recovery for as long as 24 months after surgery. Follow-up visits are periodically scheduled throughout the recovery period. Ongoing eye care is essential during the postoperative healing phase.

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Complications

The main deterrence to decompression of the facial nerve is further injury to an already traumatized nerve that prolongs or possibly prevents nerve recovery. Only surgeons experienced with surgery in the temporal bone should perform facial nerve decompression.

Additional complications include dural tears, conductive or sensorineural hearing loss, vestibular function loss, persistent CSF leaks, and meningitis. These complications can also occur secondary to temporal bone fracture alone. Dural tears and subsequent CSF leaks are most likely incurred during elevation of the middle fossa dura. Repair should be performed intraoperatively by using temporalis fascia with or without augmentation with fibrin glue.

Meningitis is a rare complication of persistent CSF leaks, occurring in approximately 8% of patients. Prophylactic antibiotics may not be effective in lowering this rate. However, antibiotics are usually given perioperatively. Conductive hearing loss can result from ossicular disruption during dissection or from temporal-lobe herniation after surgery. Direct injury to the cochlea, vestibule, semicircular canals, or internal auditory vessels may produce permanent sensorineural hearing loss and/or vestibular function loss.

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Outcome and Prognosis

Exploring the facial nerve after traumatic paralysis remains controversial. Further studies are necessary to resolve the issue over which patients should undergo decompressive surgery to recover facial nerve function.

With nonpenetrating trauma, the overall rate of good recovery (ie, House-Brackmann grade 1 or 2) after decompression of the facial nerve is traditionally 50%. Previous data suggested an equal probability of recovering good function with nonoperative management when all injuries and presentations are considered.

For example, McKennan and Chole (1992) questioned the benefit of surgery. [14] Exploratory surgery and repair was performed on 14 patients with immediate-onset complete facial paralysis. Nerve transection was found in 8 patients. However, only 4 were monitored longer than 1 year after surgery. Of the 4 patients, 2 improved to moderately severe dysfunction (ie, House-Brackmann grade 4), and the remaining 2 continued to have total paralysis (ie, House-Brackmann grade 6).

Authors of small case series such as these that lack adequate follow-up questioned the utility of surgery among patients with nerve transection. Severe injuries, such as nerve transection, were thought to carry a poor prognosis irrespective of surgical intervention and repair. With this possibility in mind, the merits of surgical decompression need further evaluation, especially when the clinically significant risks and complications of an intracranial procedure are considered.

Recent authors profess the utility of surgery in specific situations, especially when a severance of a nerve is suspected. Although the overall incidence of transection is low, the outcome is undoubtedly poor without intervention.

For example, in a prospective case series of 10 patients with 11 temporal bone fractures, decision for surgical intervention was mainly based on high-resolution CT scan and lack of regeneration potentials on EMG. In this series, no nerve transections were encountered. After surgical exploration and decompression, 5 fractures recovered to House-Brackmann (HB) grade 1, 4 patients recovered HB grade 2, and 2 patients recovered HB grade 3. [8]

In a retrospective study, Darrouzet et al (2001) examined 115 patients with posttraumatic facial paralysis. [15] Patients with immediate and electrophysiologically severe facial paralyses with a clear fracture line on the fallopian canal on CT scans were treated with surgery as soon as possible. Patients with delayed or severe facial paralyses and a mixed electrophysiologic pattern were treated medically. Patients with severe facial paralyses without a clearly visible fracture line on CT underwent electrophysiologic and clinical monitoring with the option of late surgery if they did not recover. Of 65 patients who underwent surgery, 52 (80%) had immediate severe paralysis, 2 (3%) had delayed-onset paralysis, and 11 (17%) had unknown delay-associated paralysis. Nerve transection was found in 9 patients (14%). After 2 years of follow-up, 61 patients (94%) had a grade 1-3 recovery. A grade 4 recovery was observed in 4 patients; no patients recovered to a grade 5 or 6 level.

In what appears to be a related article to this study, the functional outcome of 64 cases of facial paralysis following temporal bone fracture was better described. [9] Based on a decision algorithm combining CT scan findings and electroneuronography, 38 patients were given medical treatment and 26 underwent surgery. Normal or near-normal facial nerve recovery (HB 1-2) were obtained in 63% of medically treated patients and 39% of surgically treated patients. Grades 3-4 were obtained in 13% of medically treated patients and 42% of surgically treated cases. In addition, the authors concluded that grade 3 is the best obtainable result after nerve anastomosis.

In addition, data have also challenged the timing of surgery. Initial beliefs held that surgery should be performed within 2-3 weeks after injury. However, because most patients have multisystemic trauma, surgery for facial nerve decompression within this window is not feasible.

Quaranta et al (2001) retrospectively reviewed outcomes after late facial nerve decompression. [16] All 9 patients satisfied traditional electrophysiologic criteria and were operated on 27-90 days after trauma. Normal or near-normal (HB 1-2) facial function was achieved in 7 (78%) after more than 1 year of follow-up. The remaining 2 patients, operated on 3 months after trauma, obtained grade 3 recoveries. The authors concluded that, in patients who cannot undergo surgery early and who present at 1-3 months with more than 95% denervation on ENoG, facial nerve decompression may still be beneficial. However, studies such as this lack a control group; therefore, knowledge about the potential for recovery of such patients when treated medically or untreated is lacking.

A study by Liu et al reported good outcomes from extended subtotal facial nerve decompression performed through the transmastoid approach in patients with facial palsy after temporal bone fracture, but indicated that such surgery should be performed within 8 weeks following the causative trauma. Of the 12 patients who underwent surgery within 8 weeks of trauma, 11 of them (91.7%) achieved complete or near-complete recovery from facial palsy, while of the six patients who underwent decompression between 9 and 14 weeks after injury, only four (66.7%) attained complete or near-complete recovery. [17]

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Future and Controversies

Despite emerging studies, the management of intratemporal facial paralysis remains controversial. Data with regard to patient-selection criteria and the benefit of surgical intervention remain inconclusive.

Further controlled studies in which algorithm-based, as depicted in the image below, patient-selection criteria are used will help define the role of surgery.

Proposed algorithm for the management of intratemp Proposed algorithm for the management of intratemporal injury to the facial nerve.

Furthermore, with further improvement in CT scanning and MRI technology, imaging may allow for a noninvasive determination of the integrity of the facial nerve and/or the extent of injury. This ability might facilitate proper selection of patients who may benefit from exploration or repair of a transected facial nerve.

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