Temporal bone fractures are uncommon but involve many important structures resulting in various diagnostic and therapeutic issues. A large amount of force is required to fracture the temporal bone, so patients present with other injuries that usually take precedence comparatively. Unlike fractures in other head and neck regions, the management of temporal bone fractures is pursued to address functional deficits rather than reduction and fixation. Since the temporal bone is non-weight bearing, cosmetic sequelae are rare secondary to this trauma. However, functional deficits from facial nerve dysfunction can be devastating to a patient from not only a functional perspective but also as a cosmetic issue.
Overall, in the adult population, most temporal bone fractures result from motor vehicle accidents followed by assault and falls. Regarding pediatric patients, 30% result from motor vehicle accidents compared to 60% from falls.
Temporal bone fractures have been reported across all age groups as trauma affects each age group. However, 70% of these fractures occur within the second through fourth decades of life with a 3 to 1 male to female predominance.
Generally, temporal bone fractures are secondary to trauma of some kind. The force required to fracture the temporal bone is 1875 lbs. Temporal bone fractures are no longer classified as longitudinal or transverse but rather otic capsule sparing or otic capsule disrupting.
Otic sparing fractures travel from the squamosal portion of the temporal bone and the posterosuperior wall of the external auditory canal. The fracture passes through the mastoid air cells and middle ear and then fractures the tegmen mastoideum and tegmen tympani or roof of mastoid air cells or middle ear, respectively. These fractures typically result from a blow to the temporoparietal region.
Otic capsule-disrupting fractures pass through the otic capsule and proceed from foramen magnum to petrous pyramid and capsule. These fractures do not typically affect the ossicular chain or the external auditory canal but almost always result in sensorineural hearing loss (25 times more likely) and are eight times more likely to result in cerebrospinal fluid (CSF) otorrhea.
On clinical evaluation, all aspects of otologic examination are important. Beginning first with the auricle, one must check for auricular hematomas that may need to be decompressed or if there is exposed auricular cartilage that may need to be covered to prevent chondritis.
Examination of the ear canal will reveal any fractures into the external auditory canal or the presence of cerebrospinal fluid otorrhea. There is no need to pack the external ear canal unless it is required to control significant hemorrhage. If profuse hemorrhage cannot be controlled with packing, the patient may need to be taken to the operating room for carotid ligation or angiography for balloon occlusion.
Next, an examination of the tympanic membrane should evaluate if it is still intact or perforation. Bloody otorrhea or hemotympanum are the two most common signs of temporal bone fracture. Generally, hemotympanum is self-resolving within 4 to 6 weeks. Traumatic tympanic membrane perforations may heal spontaneously, pending their overall size.
Hearing is initially assessed at the bedside via tuning fork examination with a 512-Hertz tuning fork. Both Weber and Rinne tests are useful to determine if a conductive or sensorineural hearing loss is present. In the presence of facial paralysis or cerebrospinal fluid fistula where operative management is paramount, preoperative audiometry is necessary.
The vestibular system is contained within the temporal bone and should also be routinely evaluated in the presence of a temporal bone injury. Neurologic injuries such as concussions, contusions, or other injuries to the brainstem and cerebellar pathways may coexist with the otic capsule involved injuries. A bedside vestibular evaluation should be performed in addition to the neurologic evaluation. A cervical spine injury needs to be ruled out before any vestibular evaluation can be performed. Evaluation should include spontaneous or gaze-evoked nystagmus, gait abnormalities, Dix-Hallpike test to evaluate for benign paroxysmal positional vertigo, head thrust nystagmus for refixation saccade, and assessment of post-head-shake nystagmus. The most common injury to the vestibular system would include benign paroxysmal positional vertigo (BPPV) and vestibular hypofunction.
Assessment of the facial nerve as early as is possible is very important, and baseline function should be established before paralysis or intubation. Assessment of each distal branch and bilaterally comparison should be performed to determine if paresis or paralysis is present. Careful attention to eye closure is important as one will want to avoid exposure keratitis. If the patient is uncooperative, unconscious, or sedated, inducing pain may be one method of stimulated facial movement. Of note, a patient with paralysis may appear to have limited function, but it is passive movement from the uninvolved side. If this is suspected, the examiner should physically restrict movement on the normal side by pressing the overlying facial soft tissue and reassessing for movement on the injured side.
High-resolution computed tomography (CT) is the gold standard for diagnosis and classification of temporal bone fractures. CT scans should be ordered in the presence of facial paralysis, cerebrospinal fluid fistula, disruption of the superior wall of the external auditory canal, or scutum with potential trapping of epithelium, suspected vascular injury, or when surgical intervention is required for management of otologic complication. Hearing loss in the absence of other complications does not warrant CT. If a vascular injury is suspected, CT angiography is better than a non-angiographic CT.
Regarding the facial nerve, the House-Brackmann scale is used to evaluate and grade overall facial nerve function on a subjective, clinical basis.
For an objective assessment of the facial nerve, electrophysiologic testing is available.
Electroneuronography is the most accurate, qualitative measurement. This test is ordered if unilateral complete facial paralysis, or House-Brackmann grade VI, is present. This test requires a contralateral intact side for comparison. Electroneuronography is an evoked test that compared the compound action potential of the damaged side compared to the non-damaged side. Degeneration greater than 90% within six days of onset have a poorer outcome for spontaneous recovery. This test is ordered between 3 to 14 days as one must allow for the natural Wallerian degeneration of the nerve before ordering. Early testing may, therefore, produce erroneous results as degeneration is not complete and why serial electroneuronography is performed — also, no benefit to intervention after 14 days.
Electromyography is not used for interventional purposes but is a quantitative analysis for prognosis usually performed after 14 days. Normal muscle is electrically silent, but after 10 to 14 days, the denervated muscle begins to fire spontaneously with loss of voluntary potentials. Diphasic or polyphasic potentials indicate a good prognosis while fibrillations, signaling loss of voluntary potentials, is a poorer prognosis.
If there is clear fluid coming from the ear canal or into the nasal cavity, diagnostic testing of the otorrhea and rhinorrhea can reveal CSF present. Fluid sampling will reveal that CSF has a higher glucose content but a lower protein and potassium content than mucosal secretions. Testing of the fluid for beta-2 transferrin is specific for CSF.
Indications for surgery of a temporal bone fracture include:
The primary surgical objections of reconstruction include:
If the patient has intact hearing, middle cranial fossa, and transmastoid approaches can be used to decompress the facial nerve. A facial recess approach will help provide examination of the nerve from the geniculate ganglion to the second genus. If the fracture and site of compression are lateral to the geniculate ganglion, the transmastoid approach can be used. If the patient does not have intact hearing, a transmastoid-translabyrinthine approach can be used.
Given that the diagnosis is made via CT imaging, the clinical exam must rule out CSF otorrhea or CSF rhinorrhea.
Overall, many temporal bone fracture patients will have a good prognosis. Most facial nerve paresis, paralysis will resolve on its own unless it is House-Brackmann grade VI injury. Per Brodie and Thompson, patients that presented with normal facial nerve function on the initial exam that progressed to complete paralysis recovered to a House-Brackmann I or II.
In the absence of CSF leak, prophylactic antibiotics are not indicated in temporal bone fractures. Per Brodie and Thompson, there is an incidence of less than 1% of meningitis in patients without CSF leak.
Temporal bone injuries can result in conductive, sensorineural, or mixed hearing loss. Systemic steroids should be considered for patients with sensorineural hearing loss (SNHL) or mixed hearing loss to decrease nerve inflammation. Many surgical procedures can be considered to repair tympanic membrane loss, ossicular discontinuity, or other types of conductive hearing loss.
Patients that present with an injury to the external auditory canal are at risk for the development of cholesteatoma secondary to entrapping of the epithelium. Obvious entrapment present should be surgically repaired via mastoidectomy and/or canaloplasty to debride, remove epithelium and then reconstruct. Some patients can be observed via serial CT scans to ensure no trapping of the epithelium. A late complication of temporal bone fractures is external auditory canal stenosis.
Severe injury of the tegmen, or roof of the middle ear or mastoid, may result in the late development of brain herniation into the middle ear. This is called either an encephalocele or meningocele, which happens secondary to the weight of the temporal lobe and intracranial pressure. A usual presentation will be a CSF leak, conductive hearing loss (CHL), or meningitis. CT scans confirm the diagnosis. Patients will need a surgical repair via transmastoid and middle cranial fossa approach.
Due to the disruption of mucosal anatomical barriers naturally present, meningitis is a late complication. Infection occurs via the spread of otitis media through the otic capsule into the intracranial space.
As stated above, patients will need close follow up to rule out late complications such as meningitis, entrapped epithelium leading to cholesteatoma formation, facial nerve serial monitoring, or postsurgical follow up if facial nerve decompression was necessary.
As temporal bone fractures are not isolated trauma, a trauma team consultation is necessary as there are most likely other injuries outside the scope of otolaryngology. If the fracture results in neurologic dysfunction, a neurosurgery consultation may be necessary as brain tissue may be involved.
Patients who are clinically observed without full paralysis need to be educated that their facial nerve function may fully recover or only partially recover. Anytime steroids are prescribed, patients should be educated regarding the potential side effects of steroids use as well.
Temporal bone fractures are often seen in the emergency department, but their management requires an interprofessional team that includes a neurologist, specialty nurses, trauma surgeon, neurosurgeon, otolaryngologist, and intensivist. Most of these fractures are associated with concomitant injury to the face, spine, and chest, and hence, the appropriate specialist should be involved. Trauma and critical care monitor patients and notify the team of changes. Besides the injury to the facial nerve, other complications include CSF leak, meningitis, and cholesteatoma formation. For undisplaced temporal bone fractures, the prognosis is good, but displaced fractures with nerve entrapment do require surgical decompression. The surgery is often associated with complications, and recovery is prolonged.
|||Temporal bone fractures. Review of 90 cases., Cannon CR,Jahrsdoerfer RA,, Archives of otolaryngology (Chicago, Ill. : 1960), 1983 May [PubMed PMID: 6847478]|
|||Management of complications from 820 temporal bone fractures., Brodie HA,Thompson TC,, The American journal of otology, 1997 Mar [PubMed PMID: 9093676]|
|||Feng Y,Patel NS,Burrows AM,Lane JI,Raghunathan A,Van Gompel JJ,Carlson ML, Expansile Traumatic Neuroma of the Intratemporal Facial Nerve. Journal of neurological surgery reports. 2019 Jan; [PubMed PMID: 30941279]|
|||Gordin E,Lee TS,Ducic Y,Arnaoutakis D, Facial nerve trauma: evaluation and considerations in management. Craniomaxillofacial trauma [PubMed PMID: 25709748]|
|||Vashishth A,Singh Nagar TR,Mandal S,Venkatachalam VP, Extensive intratemporal cholesteatomas: presentation, complications and surgical outcomes. European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery. 2015 Feb; [PubMed PMID: 24318471]|
|||Allen KP,Hatanpaa KJ,Lemeshev Y,Isaacson B,Kutz JW, Intratemporal traumatic neuromas of the facial nerve: evidence for multiple etiologies. Otology [PubMed PMID: 24270721]|
|||Nash JJ,Friedland DR,Boorsma KJ,Rhee JS, Management and outcomes of facial paralysis from intratemporal blunt trauma: a systematic review. The Laryngoscope. 2010; [PubMed PMID: 21225812]|
|||Kim J,Moon IS,Shim DB,Lee WS, The effect of surgical timing on functional outcomes of traumatic facial nerve paralysis. The Journal of trauma. 2010 Apr; [PubMed PMID: 20032793]|
|||Results of decompression with middle cranial fossa approach or traumatic intratemporal fascial nerve injury., Aslan H,Songu M,Eren E,Başoğlu MS,Özkul Y,Ateş D,Katilmiş H,Güvenç G,, The Journal of craniofacial surgery, 2014 Jul [PubMed PMID: 25006913]|
|||Management and outcomes of facial paralysis from intratemporal blunt trauma: a systematic review., Nash JJ,Friedland DR,Boorsma KJ,Rhee JS,, The Laryngoscope, 2010 Jul [PubMed PMID: 20564723]|
|||Patel A,Groppo E, Management of temporal bone trauma. Craniomaxillofacial trauma [PubMed PMID: 22110824]|